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Bacterial endotoxin is considered as one of the critical risk factors in medical devices, especially implanted devices that directly or indirectly contact with blood circulating system. In that case, endotoxin limits for implanted medical devices is important in determine the safety of medical devices. According to GB/T 14233.2-2005, the requirements of endotoxin index for intrathoracic medical devices is 2.15 EU per device. However, the definition of "intrathoracic medical devices" is vague. Specifically, "for cardiovascular system application" instead of "intrathoracic application" is more reasonable. With the deeper understanding of the risk of endotoxin in medical devices and considering the internationally accepted standards, the limits of endotoxin in medical devices for cardiovascular system application is acceptable at 20 EU per device.
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EndotoxinsABSTRACT
Objective:To analyze the current status of frailty in elderly patients undergoing cardiac surgery, explore its risk factors, and establish a predictive model of frailty in order to provide targeted and predictive nursing programs.Methods:A total of 205 cardiac surgery patients admitted to the first affiliated hospital of Xinjiang Medical University from March 2015 to January 2019 were selected as the study subjects. Patients were divided into 2 groups according to whether they were frail: the frailty group ( n=78) and the control group ( n=127). Logistic regression was used to analyze the risk factors that affect the frailty of elderly patients undergoing cardiac surgery. The receiver operating characteristic curve (ROC) was used to evaluate the effectiveness of model X [consisting of body mass index (BMI), Mini-Mental State Examination (MMSE) score, number of diseased patients, and number of drugs] in diagnosing frailty in elderly patients undergoing cardiac surgery. Results:Of the 205 patients, 78 (38.05%) showed frailty. The proportion of high school education level and above, Tinetti Gaitassessment (TGA) score≥24 and MMSE score≥27 in the frailty group was lower than that in the control group, and the proportion of Geriatric Depression Scale-15 (GDS-15) score≥7, the number of diseases≥3 and the number of drugs≥5 in the frailty group was higher than that in the control group ( χ2 value was 9.254-26.061, P<0.05). Logistic regression analysis showed that BMI, MMSE score, number of diseased, and number of medications were independent risk factors for frailty in elderly patients undergoing cardiac surgery ( OR value was 0.032-5.275, P<0.05). The area under the ROC curve, sensitivity and specificity of frailty in elderly cardiac surgery patients assessed by model X were 0.913, 75.61% and 96.77%, respectively. Conclusion:The incidence of frailty is higher in elderly patients undergoing cardiac surgery. Model X can diagnose the frailty of elderly patients undergoing cardiac surgery and help clinical nurses to carry out targeted care.
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Objective The aims of this study were to investigate the expression of microRNA-30a(miR-30a)in human bladder cancer cell lines and their effects on the proliferation,apoptosis and migration of human bladder cancer cells.Methods The expression levels of miR-30a in bladder cancer cell lines(5637 and T24)and bladder epithelial immortalized cells(SV-HUC-1)were detected by real-time quantitative PCR(qRT-PCR).The expression of miR-30a was up-regulated or down-regulated by T24 cells transfected with miR-30a mimic or 5637 cells transfected with miR-30a inhibitors and controls using NC mimic or NC inhibitor.The effects of miR-30a expression on the proliferation,apoptosis and invasion of bladder cancer cells were investigated by flow cytometry,MTT and Transwell assays.Results The expression level of miR-30a in two bladder cancer T24 and 5637 cell lines was significantly lower than that in normal bladder SV-HUC-1 cell line(P<0.05),and the expression level of miR-30a was lower in the high degree of malignancy in bladder cancer T24 cells than that in malignant degree of relatively low 5637 cells.After 72h transfection,the values of optical density(OD)in the miR-30a mimic group(0.83±0.09)was significantly lower than that in NC mimic group(1.21±0.12)in T24 cells(P<0.01).The OD values of miR-30a inhibitor group(1.28±0.14)was significantly lower than that in the NC inhibitor group(1.09±0.14)in 5637 cells(P<0.01).The apoptotic rate of miR-30a mimic group in T24 cells(21.27±2.42)% was significantly higher than that in the NC mimic group(10.61±1.29)%(P<0.01).The apoptotic rate of the miR-30a inhibitor group in 5637 cells(6.78±2.57)% was significantly lower than that in the NC mimic group(13.42±1.40)%(P<0.01).The number of transmembrane cells in miR-30a mimic group in T24 cells(183.57±16.61)was significantly lower than that in NC mimic group(465.80±9.20)(P<0.01).The number of transmembrane cells in the miR-30a inhibitor group in 5637 cells(581.25±11.02)was significantly lower than that in NC mimic group(397.13±7.57)(P<0.01).Conclusion Up-regulation of miR-30a can inhibit the proliferation of bladder cancer cells,promote cell apoptosis and reduce the ability of migration and invasion in bladder cancer cells.The low expression of miR-30a in bladder cancer cells may be related to the development and metastasis in bladder cancer.
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Objective:To study the influence of chloroquine combined with decitabine in the apoptosis of leukemia K562 cells and KG-1a1Aor1a cells,to explore the effect of autophagy on the leukemia cell apoptosis induced by decitabine,and to clarify its mechanism.Methods:The leukemia K562 and KG-1a1Aor1a cells were cultivated in vitro and divided into blank control group,decitabine group (10 μmol · L 1) and chloroquine (50 μmol · L 1) combined with decitabine group (combined group).The leukemia cells in combined group were pre-treated with chloroquine for 6 h before experiment.After treatment with drugs for 24 and 48 h,the number of cells was detected and by CCK-8 method the inhibitory rates of proliferation cells were calculated;the apoptotic rates and mitochondrial membrane potential were detected by flow cytometry.Q-PCR method was carried out to determine the gene expression levels of Atg7 and Atg12,and Western blotting was used to test the protein expression of LC3.Results:After treatment for 24 and 48 h,the number of K562 and KG-1a1Aor1a cells in decitabine group and combined group were decreased compared with blank control group (P＜0.05 or P＜0.01);the apoptotic rates and mitochondrial membrane potential were remarkably increased (P＜0.05 or P＜0.01).Compared with decitabine group,the number of K562 and KG-1a1Aor1a in combined group was significantly decreased,and the apoptotic rates were remarkably increased (P＜0.05).After treatment for 24 h,the expression levels of Atg7,Atg12 and LC3-Ⅱ/LC3-Ⅰ in the leukemia K562 and KG-1a1Aor1a cells in decitabine group were significantly increased compared with blank control group (P＜0.05 or P＜0.01);the expression levels of Atg7,Atg12 and LC3-Ⅱ/LC3-Ⅰ in the leukemia K562 and KG-1a1Aor1a cells in combined group were significantly decreased compared with decitabine group (P＜0.05 or P＜0.01).Conclusion:Decitabine could promote the apoptosis of leukemia cells,and the inhibition of autophagy by chloroquine can promote the apoptosis induced by decitabine.
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Objective:To study the influence of chloroquine combined with decitabine in the apoptosis of leukemia K562 cells and KG-1a1Aor1a cells,to explore the effect of autophagy on the leukemia cell apoptosis induced by decitabine,and to clarify its mechanism.Methods:The leukemia K562 and KG-1a1Aor1a cells were cultivated in vitro and divided into blank control group,decitabine group (10 μmol · L 1) and chloroquine (50 μmol · L 1) combined with decitabine group (combined group).The leukemia cells in combined group were pre-treated with chloroquine for 6 h before experiment.After treatment with drugs for 24 and 48 h,the number of cells was detected and by CCK-8 method the inhibitory rates of proliferation cells were calculated;the apoptotic rates and mitochondrial membrane potential were detected by flow cytometry.Q-PCR method was carried out to determine the gene expression levels of Atg7 and Atg12,and Western blotting was used to test the protein expression of LC3.Results:After treatment for 24 and 48 h,the number of K562 and KG-1a1Aor1a cells in decitabine group and combined group were decreased compared with blank control group (P＜0.05 or P＜0.01);the apoptotic rates and mitochondrial membrane potential were remarkably increased (P＜0.05 or P＜0.01).Compared with decitabine group,the number of K562 and KG-1a1Aor1a in combined group was significantly decreased,and the apoptotic rates were remarkably increased (P＜0.05).After treatment for 24 h,the expression levels of Atg7,Atg12 and LC3-Ⅱ/LC3-Ⅰ in the leukemia K562 and KG-1a1Aor1a cells in decitabine group were significantly increased compared with blank control group (P＜0.05 or P＜0.01);the expression levels of Atg7,Atg12 and LC3-Ⅱ/LC3-Ⅰ in the leukemia K562 and KG-1a1Aor1a cells in combined group were significantly decreased compared with decitabine group (P＜0.05 or P＜0.01).Conclusion:Decitabine could promote the apoptosis of leukemia cells,and the inhibition of autophagy by chloroquine can promote the apoptosis induced by decitabine.
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BACKGROUND:Cytotoxicity of graphene oxide to normal cel s is relatively low, but whether graphene oxide loaded with doxorubicin has some effects on malignant cel s is rarely reported. OBJECTIVE:To explore the cytotoxicity of graphene oxide loaded with doxorubicin on multiple myeloma cel s. METHODS:Multiple myeloma cel line RPMI8226 in logarithmic phase was selected, cultured and divided into four groups, including graphene oxide loaded with doxorubicin, doxorubicin and graphene oxide groups as wel as control group with no intervention. After 24 hours of culture, the cel activity was detected by cel counting kit-8 method, and the cel cycle and apoptosis were detected using flow cytometry. RESULTS AND CONCLUSION:Plump-shaped cel s with translucent and clear cytoplasm were found in the control group;cel s with relatively translucent cytoplasm, and even a few shrunken cel s appeared in the graphene oxide group;cel ular morphology was in a heterogeneity, apoptotic bodies appeared in the doxorubicin group;the cel s was significantly reduced in size, presenting more obvious shrinkage and apoptotic bodies in the group of graphene oxide loaded with doxorubicin. The cel survival rate in the graphene oxide loaded with doxorubicin, doxorubicin and graphene oxide groups was significantly lower than that in the control group (P<0.05), and this indicator was significantly lower in the group of graphene oxide loaded with doxorubicin than the graphene oxide group (P<0.05). The apoptotic rate in the group of graphene oxide loaded with doxorubicin and doxorubicin group was significantly higher than those in the graphene oxide and control groups (P<0.05), respectively. Additional y, there were no significant differences in the cel cycle among groups. These results show that graphene oxide loaded with doxorubicin has a stronger cytotoxicity, and can induce apoptosis in human multiple myeloma cel s.
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Objective To evaluate the impact of vagal denervation (VD) that is derived from circumferential ablation of pulmonary vein ostium for paroxysmal atrial fibrillation (AF) on the therapeutic results. Methods A total of 50 patients with paroxysmal atrial fibrillation were enrolled in this study. Circumferential ablation of pulmonary vein ostium was carried out in all the patients. The end point of ablation was pulmonary vein electricity isolation. The patients in whom VD occurred during the performance of ablation were regarded as VD- positive group (n = 19), and the remaining patients were used as VD- negative group (n = 31). The recurrence rate of AF six months after the treatment was recorded, and the results were compared between the two groups. Results The end point of ablation was successfully achieved in all the fifty cases. Six months after the ablation, the therapeutic effect of VD- positive group was significantly better than that of VD- negative group (84.21% vs 64.51%, P ≤ 0.05). Conclusion The vagal denervation effect that is derived from circumferential ablation of pulmonary vein ostium in treating AF can significantly increase the success rate of radiofrequency ablation for AF.
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According to the clinical needs of precise radiotherapy, an integrative thermoplastic immobilization board for radiotherapy was developed for the purpose of immobilizing head position, head, neck and shoulder positions and body position respectively. The new style board has several characteristics: a board with multi-purposes, ease of handling and good accuracy of patients' positions, etc.
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Humans , Equipment Design , Immobilization , Posture , RadiotherapyABSTRACT
Objective To explore effect on the proliferation and apoptosis of Hela cells in vitro by using vascular endothelial growth factor-C(VEGF-C) antisense oligonucleotides (ASODN). Methods VEGF-C ASODN was transfected into Hela cells by liposome-mediated; the cells transfected with the oligodeoxynuclecotide (SODN) and saline were used as control groups. The efficiency of transfection was detected by fluorescence microscope. The inhibitive rate of cell growth was detected with MTT methods. Apoptosis and cell cycle were evaluated using FCM. The mRNA expression of VEGF-C was determined by RT-PCR, and the expression of VEGF-C was determined by western blotting. Results VEGF-C ASODN had been transfected into Hela cells by liposome-mediated. The index of apoptosis after transfection 48 h was (19.39±1.81)%. G2/M phase cell increased after transfection, meanwhile the expression of VEGF-C degraded on the level of mRNA and protein (P<0.05). Conclusion Transfeeted with VEGF-C ASODN could down-regulate the expression of VEGF on the level of mRNA and protein, block the cell circle, inhibit cell proliferation and induce apoptosis in Hela cells in vitro.
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Background and purpose: NF-?B is activated by tumor necrosis factor,some chemotherapeutic agents,and ionizing radiation.The activation of NF-?B could result in inhibition of apoptosis.NF-?B,regulated by PDTC(pyrrolidine dithiocarbamate),is a specific inhibitor of NF-?B.The purpose of our study was to explore the impact of inhibiting expression of NF-?B on radiation-induced apoptosis of uterine cervix cancer HeLa cells.Methods:Inhibition of NF-?B in HeLa cells was performed by treatment with 100 ?mol/L PDTC for 2 hours.Cells were irradiated at 0,2,4 and 6 Gy with or without PDTC.The expression of NF-?B in nuclear was determined by western blot,and apoptosis was evaluated by using the TUNEL assay.Cell proliferation was evaluated by using MTT assay.Results:NF-?B activation was induced by radiation and inhibited by PDTC.Inhibition of radiation-induced NF-?B activation resulted in inhibiting cell proliferation(P