Bone Transplantation/adverse effects* ; Transplantation, Autologous/adverse effects*

Objective:To investigate the correlation between plasma microRNA (miR)-122, miR-33a and the severity of coronary artery disease in patients with type 2 diabetes mellitus (T2DM) and coronary heart disease.Methods:The clinical data of 196 patients with T2DM from January 2019 to October 2021 in Xuzhou First People′s Hospital were retrospectively analyzed. Among them, 81 cases were complicated with coronary heart disease (combined group), 115 cases were not complicated with coronary heart disease (control group). The plasma levels of miR-122 and miR-33a were detected by real-time fluorescence quantitative reverse transcription polymerase chain reaction, the plasma level of N-terminal B-type natriuretic peptide precursor (NT-proBNP) was detected by enzyme-linked immunosorbent assay. In combined group, the number of coronary artery lesions was determined according to the results of coronary angiography, and Gensini score was evaluated. Linear regression model was used to analyze the relationship between plasma miR-122, miR-33a and NT-proBNP levels with the incidence of coronary heart disease in patients with T2DM. Receiver operating characteristic (ROC) curve was used to analyze the plasma miR-122 and miR-33a in predicting efficiency of coronary heart disease in patients with T2DM. In combined group, Spearman correlation method was used to analyze the relationship between plasma miR-122, miR-33a and the number of coronary artery lesions, and Pearson correlation method was used to analyze the relationship between plasma miR-122, miR-33a and plasma NT proBNP, Gensini score.Results:The plasma miR-122, miR-33a and NT-proBNP in combined group were significantly higher than those in control group: 5.76 ± 1.35 vs. 1.18 ± 0.33, 1.39 ± 0.37 vs. 0.65 ± 0.11 and (786.87 ± 156.39) ng/L vs. (103.45 ± 19.27) ng/L respectively, and there were statistical differences ( P<0.01). Linear regression result showed that plasma miR-122, miR-33a, and NT-proBNP were positive correlation with occurrence of coronary heart disease in patients with T2DM ( P<0.01); ROC curve analysis result showed that the area under curve of plasma miR-122, miR-33a and combination in predicting coronary heart disease in patients with T2DM were 0.816, 0.845 and 0.912 respectively (95% CI 0.744 to 0.865, 0.768 to 0.892 and 0.836 to 0.967). Coronary angiography result showed that there were 46 cases of single vessel lesions, 25 cases of double vessel lesions and 10 cases of three vessel lesions. The plasma miR-122, miR-33a, NT-proBNP and Gensini score in patients with three vessel lesions were significantly higher than those in patients with double vessel lesions and patients with single vessel lesions: 6.52 ± 0.96 vs. 4.95 ± 0.85 and 3.74 ± 0.52, 1.45 ± 0.31 vs. 1.06 ± 0.25 and 0.81 ± 0.13, (829.78 ± 62.59) ng/L vs. (627.48 ± 47.12) and (502.64 ± 38.24) ng/L, (63.89 ± 12.71) scores vs. (42.18 ± 6.03) and (22.36 ± 2.41) scores, the indexes in patients with double vessel lesions were significantly higher than those in patients with single vessel lesions, and there were statistical differences ( P<0.05). In combined group, Spearman correlation analysis result showed that the plasma miR-122 and miR-33a were positive correlation with the number of coronary artery lesions ( r = 0.879 and 0.825, P<0.05); Pearson correlation analysis result showed that the plasma miR-122 and miR-33a were positive correlation with the plasma NT-proBNP and Gensini score (miR-122: r = 0.896 and 0.788, miR-33a: r = 0.871 and 0.765; P<0.05). Conclusions:The plasma levels of miR-122 and miR-33a are related to the occurrence of coronary heart disease and severity of coronary artery disease in patients with T2DM, which may be used to guide the prevention and treatment of coronary heart disease in patients with T2DM.

Objective:To construct a multi-stage dynamic prevention and control model, establish a system of intervention points and prevention and control measures for the prevention and control of workplace violence in hospitals, so as to provide guidance for hospitals and medical staffs to effectively prevent and respond to such incidents.Methods:Based on the crisis management theory, a model for the prevention and control of workplace violence in hospitals was constructed, the intervention points and prevention and control measures were screened by the Delphi method.Results:A multi-stage dynamic prevention and control model of workplace violence in hospitals was constructed, and a system of intervention points and prevention and control measures for workplace violence in hospitals were established according to the model. The system was divided into three stages: the pre-event stage contained 10 intervention points and 48 countermeasures, the in-event stage contained 6 intervention points and 17 countermeasures, and the post-event stage contained 3 intervention points and 12 countermeasures.Conclusions:It is an effective way to avoid violence and reduce the damage degree of violent incidents by selecting different countermeasures for different intervention points and carrying out multi-stage dynamic prevention and control of workplace violence in hospitals.

Venous thromboembolism (VTE) is one of the common complications of lung adenocarci-noma. The state of the driver genes of lung adenocarcinoma is related to the risk of VTE. The common driver genes include epidermal growth factor receptor, anaplastic lymphoma kinase, c-ros oncogene 1 receptor kinase and Kirsten rat sarcoma viral oncogene, etc.. Based on the study of the correlation between lung adenocarci-noma driver genes and VTE, it is of great significance for the early clinical prevention of VTE in patients with lung adenocarcinoma to screen out patients with high risk of VTE according to the state of the driver genes and finally evaluate the risk of VTE in patients with lung adenocarcinoma by combining conventional risk factors with the driver genes.

Objective To investigate the dynamic changes in the nature of the pleural effusion via Light criteria in hypothermic rats induced by seawater immersion and analyze possible mechanism involved.Methods One hundred male Sprague-Dawley rats were randomly divided into the normal control group (without any treatment) and hypothermia group exposed to 20 ℃ seawater for 24 hours.Then,the hypothermia group was sub-divided into the passive rewarming groups 1,2,3 and 4 and warm water bath active rewarming groups 1,2,3 and 4,each consisting of 10 animals.The passive rewarming groups had passive rewarming after exposure to 20 ℃ seawater for 24 hours,while the active rewarming groups had warm water bath rewarming following exposure to 20 ℃ seawater for 24 hours.Then,all the animals in the sub-groups were executed 0,3,6 and 12 hours after rewarming.Serum,pleural effusion,total protein (TP) in pleural effusion,concentrations of lung homogenate lactate dehydrogenase (LDH) were measured,and Light criteria were calculated.Results There was no significant pleural effusion in the normal rats.LDH level in hypothermia-induced pleural effusion was higher than that in normal serum LDH,pleural effusion/total serum protein ratio (TPR) was lower than 0.5,and lactate dehydrogenase ratio (LDHR) was lower than 0.6.After rewarming,the amount of hypothermia-induced pleural effusion decreased gradually,while the levels of TPR and LDHR increased gradually.However,changes of LDH in pleural effusion were different with those in serum and lung homogenate.The warm water bath rewarming in the absorption of hypothermic pleural effusion was faster than passive rewarming,Warm water bath rewarming seemed to promote absorption of hypothermia-induced pleural effusion,but without statistical significance.Conclusions The 3 values of the pleural effusion criteria in hypothermic rats continuously increased following rewarming and reached the standards of effusion fluid,which did not necessarily reflect the seriousness of inflammatory pleural damage.The possible mechanism involved might be associated with the decrease of pleural effusion after rewarming,and water absorption by the body might be greater than protein absorption.

Objective To establish hypothermia SD rat model induced by prolonged seawater immersion and to observe pathological damage to vital organs as well as certain important hematological parameters .Methods Twenty male adult Sprague-Dawley rats were randomly and equally divided into the normal control group and the hypothermia experimental group ( or simply the hypothermia group ) , each consisting of 10 rats.The control group was left there without any treatment , while the hypothermia group was immersed in artificial seawater at 20 ℃ for 24 hours to observe changes in vital signs of the rats during cold seawater immersion .At the end of the experiment , body temperature , general hematological parameters and pathological changes of vital organs were detected for further study .Results During the course of cold seawater immersion, the vital signs of the rats in the hypothermia group gradually worsened [( Heart rate before immersion (369 ±25.1) beats/min] vs (126.5 ±8.6) beats/min after immersion] (P<0.05).Respiratory rate before immersion was (92.8 ±7.2) times/min vs (43.9 ±3.8) times/min after immersion (P<0.05). Rectal temperature before immersion was (37.3 ±0.3) ℃vs (21.9 ±0.8) ℃ after immersion (P<0.05). After immersion, the blood routine detection indicated that hemoglobin level of the normal control group was (145.4 ±11.5) g/L, while that of the hypothermia group was (129.5 ±12.1) g/L ( P<0.05); neutrophil percentage of the normal control group was (18.3 ±3.5) ％, while that of the hypothermia group was (34.9 ± 6.1) ％(P<0.05).Prothrombin time (PT) of the normal control group was (11.42 ±2.36) s, while that of the hypothermia group was (17.86 ±2.41) s (P<0.05); APTT of the normal control group was (12.97 ± 2.41) s while that of the hypothermia group was (17.28 ±2.33) s (P <0.05).As for biochemical parameters, alanine aminotransferase (ALT) of the normal control group was (70.40 ±15.48) U/L, while that of the hypothermia group was (183.00 ±61.62) U/L (P<0.05); aspartate transaminase (AST) of the normal control group was (115.1 ±14.8) U/L, while that of the hypothermia group was (722.3 ±248.2) U/L (P<0.05);blood urea nitrogen (BUN) of the normal control group was (9.08 ±2.44) mmol/L, while that of the hypothermia group was (21.45 ±3.43) mmol/L (P<0.05);creatinine of the normal control group was (24.71 ±6.27) μmol/L, while that of the hypothermia group was (28.08 ±5.19) μmol/L (P<0.05);CK-MB of the normal control group was (451.00 ±266.53) U/L, while that of the hypothermia group was (2854.4 ±1089.6) U/L, with significant differences (P<0.05).Pathological detection indicated that there were lesions to various extents in all the vital organs , with the lesions to the lungs and stomach being most serious, and pleural effusion induced by hypothermia was also present .Conclusion The SD rat model of hypothermia induced by prolonged seawater immersion was successfully established for subsequent studies .Our present study showed that lungs and stomach were important target organs involved in prolonged seawater immersion.

Objective To observe changes in blood biochemistry and coagulation function before and after warm water bath rewarming in SD rats with hypothermia induced by prolonged seawater immersion . Methods One hundred male Sprague-Dawley rats were randomly divided into the normal control group ( the NC group, without any treatment ) and the hypothermia group ( the HT group, exposed to seawater immersion at 20 ℃for 24 hours).The passive rewarming sub-groups (the pR group 1, 2, 3 and 4, n=10) (exposed to seawater immersion at 20 ℃for 24 hours +passive rewarming ) were respectively executed after rewarming at hour 0, hour 3, hour 6, and hour 12).The warm-water bath rewarming sub-groups (the wR group 1, 2, 3 and 4, n=10 ) ( exposed to seawater immersion at 20 ℃ for 24 hours +warm-water bath rewarming ) were respectively executed after rewarming at hour 0, hour 3, hour 6, and hour 12).Blood samples were taken from abdominal aorta for biochemical and coagulation detection .Results Zero to 3 hours after warm water bath rewarming , important parameters of hepatic and renal functions , as well as myocardial enzymes in the SD rats with hypothermia induced by prolonged seawater immersion remained at high levels or even increased to some extent.Only after 6 hours after rewarming , the above-mentioned parameters dropped considerably .However, coagulation indicators began to decline immediately after rewarming , and as compared with the passive rewarming , warm water bath rewarming could produce obviously better effects on the alleviation of abnormal hepatic and renal functions, as well as myocardial enzyme parameters (P<0.05).Conclusion Warm water bath rewarming could produce better effects on the recovery of serum biochemical parameters in rats with hypothermia induced by prolonged seawater immersion when compared with those of passive rewarming .

Objective To investigate the dynamic changes in the nature of the pleural effusion via Light criteria in hypothermic rats induced by seawater immersion and analyze possible mechanism involved.Methods One hundred male Sprague-Dawley rats were randomly divided into the normal control group (without any treatment) and hypothermia group exposed to 20 ℃ seawater for 24 hours.Then,the hypothermia group was sub-divided into the passive rewarming groups 1,2,3 and 4 and warm water bath active rewarming groups 1,2,3 and 4,each consisting of 10 animals.The passive rewarming groups had passive rewarming after exposure to 20 ℃ seawater for 24 hours,while the active rewarming groups had warm water bath rewarming following exposure to 20 ℃ seawater for 24 hours.Then,all the animals in the sub-groups were executed 0,3,6 and 12 hours after rewarming.Serum,pleural effusion,total protein (TP) in pleural effusion,concentrations of lung homogenate lactate dehydrogenase (LDH) were measured,and Light criteria were calculated.Results There was no significant pleural effusion in the normal rats.LDH level in hypothermia-induced pleural effusion was higher than that in normal serum LDH,pleural effusion/total serum protein ratio (TPR) was lower than 0.5,and lactate dehydrogenase ratio (LDHR) was lower than 0.6.After rewarming,the amount of hypothermia-induced pleural effusion decreased gradually,while the levels of TPR and LDHR increased gradually.However,changes of LDH in pleural effusion were different with those in serum and lung homogenate.The warm water bath rewarming in the absorption of hypothermic pleural effusion was faster than passive rewarming,Warm water bath rewarming seemed to promote absorption of hypothermia-induced pleural effusion,but without statistical significance.Conclusions The 3 values of the pleural effusion criteria in hypothermic rats continuously increased following rewarming and reached the standards of effusion fluid,which did not necessarily reflect the seriousness of inflammatory pleural damage.The possible mechanism involved might be associated with the decrease of pleural effusion after rewarming,and water absorption by the body might be greater than protein absorption.

Objective To establish hypothermia SD rat model induced by prolonged seawater immersion and to observe pathological damage to vital organs as well as certain important hematological parameters .Methods Twenty male adult Sprague-Dawley rats were randomly and equally divided into the normal control group and the hypothermia experimental group ( or simply the hypothermia group ) , each consisting of 10 rats.The control group was left there without any treatment , while the hypothermia group was immersed in artificial seawater at 20 ℃ for 24 hours to observe changes in vital signs of the rats during cold seawater immersion .At the end of the experiment , body temperature , general hematological parameters and pathological changes of vital organs were detected for further study .Results During the course of cold seawater immersion, the vital signs of the rats in the hypothermia group gradually worsened [( Heart rate before immersion (369 ±25.1) beats/min] vs (126.5 ±8.6) beats/min after immersion] (P<0.05).Respiratory rate before immersion was (92.8 ±7.2) times/min vs (43.9 ±3.8) times/min after immersion (P<0.05). Rectal temperature before immersion was (37.3 ±0.3) ℃vs (21.9 ±0.8) ℃ after immersion (P<0.05). After immersion, the blood routine detection indicated that hemoglobin level of the normal control group was (145.4 ±11.5) g/L, while that of the hypothermia group was (129.5 ±12.1) g/L ( P<0.05); neutrophil percentage of the normal control group was (18.3 ±3.5) ％, while that of the hypothermia group was (34.9 ± 6.1) ％(P<0.05).Prothrombin time (PT) of the normal control group was (11.42 ±2.36) s, while that of the hypothermia group was (17.86 ±2.41) s (P<0.05); APTT of the normal control group was (12.97 ± 2.41) s while that of the hypothermia group was (17.28 ±2.33) s (P <0.05).As for biochemical parameters, alanine aminotransferase (ALT) of the normal control group was (70.40 ±15.48) U/L, while that of the hypothermia group was (183.00 ±61.62) U/L (P<0.05); aspartate transaminase (AST) of the normal control group was (115.1 ±14.8) U/L, while that of the hypothermia group was (722.3 ±248.2) U/L (P<0.05);blood urea nitrogen (BUN) of the normal control group was (9.08 ±2.44) mmol/L, while that of the hypothermia group was (21.45 ±3.43) mmol/L (P<0.05);creatinine of the normal control group was (24.71 ±6.27) μmol/L, while that of the hypothermia group was (28.08 ±5.19) μmol/L (P<0.05);CK-MB of the normal control group was (451.00 ±266.53) U/L, while that of the hypothermia group was (2854.4 ±1089.6) U/L, with significant differences (P<0.05).Pathological detection indicated that there were lesions to various extents in all the vital organs , with the lesions to the lungs and stomach being most serious, and pleural effusion induced by hypothermia was also present .Conclusion The SD rat model of hypothermia induced by prolonged seawater immersion was successfully established for subsequent studies .Our present study showed that lungs and stomach were important target organs involved in prolonged seawater immersion.

Objective To observe changes in blood biochemistry and coagulation function before and after warm water bath rewarming in SD rats with hypothermia induced by prolonged seawater immersion . Methods One hundred male Sprague-Dawley rats were randomly divided into the normal control group ( the NC group, without any treatment ) and the hypothermia group ( the HT group, exposed to seawater immersion at 20 ℃for 24 hours).The passive rewarming sub-groups (the pR group 1, 2, 3 and 4, n=10) (exposed to seawater immersion at 20 ℃for 24 hours +passive rewarming ) were respectively executed after rewarming at hour 0, hour 3, hour 6, and hour 12).The warm-water bath rewarming sub-groups (the wR group 1, 2, 3 and 4, n=10 ) ( exposed to seawater immersion at 20 ℃ for 24 hours +warm-water bath rewarming ) were respectively executed after rewarming at hour 0, hour 3, hour 6, and hour 12).Blood samples were taken from abdominal aorta for biochemical and coagulation detection .Results Zero to 3 hours after warm water bath rewarming , important parameters of hepatic and renal functions , as well as myocardial enzymes in the SD rats with hypothermia induced by prolonged seawater immersion remained at high levels or even increased to some extent.Only after 6 hours after rewarming , the above-mentioned parameters dropped considerably .However, coagulation indicators began to decline immediately after rewarming , and as compared with the passive rewarming , warm water bath rewarming could produce obviously better effects on the alleviation of abnormal hepatic and renal functions, as well as myocardial enzyme parameters (P<0.05).Conclusion Warm water bath rewarming could produce better effects on the recovery of serum biochemical parameters in rats with hypothermia induced by prolonged seawater immersion when compared with those of passive rewarming .