Objective:To construct the competency evaluation index system for endoscopic specialized nurses and provide basis for training, assessment and performance evaluation of endoscopic specialized nurses.Methods:In March 2021, through literature review, research group discussion, expert interview and satisfaction questionnaire, the competency evaluation system for endoscopic specialized nurses was initially established. From March to December 2021, experts from four provinces were selected by convenient sampling for two rounds of Delphi expert consultation. The weight of each indicator was determined by the method of precedence chart and analytic hierarchy process.Results:Among two rounds of consultation, the effective recovery rates of the questionnaire were 86.36% (19/22) and 89.47% (17/19) respectively, and the authority coefficients of experts were 0.82 and 0.86 respectively. The Kendall concordance coefficients of experts' opinions on the first, second and third level indicators were 0.40, 0.50 and 0.48 respectively ( P<0.05) . The final index system included 4 first level indicators (professional knowledge, professional skills, professional development ability, personal characteristics) , 18 second level indicators and 73 third level indicators. Conclusions:The competency evaluation index system for endoscopic specialized nurses has high reliability, comprehensive and practical contents, and has certain reference significance for the management and training of endoscopic specialized nurses.

Antibiotics are playing an increasingly important role in clinical antibacterial applications. However, their abuse has also brought toxic and side effects, drug-resistant pathogens, decreased immunity and other problems. New antibacterial schemes in clinic are urgently needed. In recent years, nano-metals and their oxides have attracted wide attention due to their broad-spectrum antibacterial activity. Nano-silver, nano-copper, nano-zinc and their oxides are gradually applied in biomedical field. In this study, the classification and basic properties of nano-metallic materials such as conductivity, superplasticity, catalysis, and antibacterial activities were firstly introduced. Secondly, the common preparation techniques, including physical, chemical and biological methods, were summarized. Subsequently, four main antibacterial mechanisms, such as cell membrane, oxidative stress, DNA destruction and cell respiration reduction, were summarized. Finally, the effect of size, shape, concentration and surface chemical characteristics of nano-metals and their oxides on antibacterial effectiveness and the research status of biological safety such as cytotoxicity, genotoxicity and reproductive toxicity were reviewed. At present, although nano-metals and their oxides have been applied in medical antibacterial, cancer treatment and other clinical fields, some issues such as the development of green preparation technology, the understanding of antibacterial mechanism, the improvement of biosafety, and the expansion of application fields, require further exploration.
Oxides/chemistry* ; Metal Nanoparticles/chemistry* ; Anti-Bacterial Agents/chemistry* ; Zinc ; Copper

Objective:To investigate the mechanism of levosimendan on acute kidney injury after cardiopulmonary resuscitation (CPR) in rats.Methods:Twenty-five healthy adult male SD rats were randomly divided into three groups: control group ( n=5), levosimendan group ( n=10) and experimental group ( n=10). A cardiac arrest-cardiopulmonary resuscitation model was established using smothering method in the experimental group and levosimendan group. The levosimendan group was treated with levosimandan during and after resuscitation, while the experimental group was given equivalent volume of saline solution during and after resuscitation, and the control group was only given equivalent volume of saline without performance of CPR. The rats in the three groups were sacrificed at 6 h after resuscitation. The serum and kidney tissue samples were collected. Serum biochemical indicators [serum creatinine (Scr), blood urea nitrogen (Bun), interleukin-1β (IL-1β), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α)] were measured. HE staining and Paller score were used to identify the degree of kidney damage. Apoptosis was estimated by TUNEL staining. Western blot was used to detect the expression levels of phosphorylation of extracellular regulated protein kinases (p-ERK). One-way analysis of variance was used to compare the mean values of normally distributed measurement data between groups. Comparisons between groups were performed using the least significant difference t-test. Results:Scr (85.02±1.31) μmol/L, Bun (7.36±0.13) mmol/L, Paller score (7.3±0.2), IL-1β (302.20±17.35) pg/mL, IL-6 (564.60±23.24) pg/mL and TNF-α (1346±83.73) pg/mL in the experimental group were significantly higher than those of the control group [(15.94±0.96) μmol/L, (2.95±0.18) mmol/L, (0.7±0.2), (7.27±0.44) pg/mL, (51.30±2.87) pg/mL, and (10.39±0.52) pg/mL] (all P<0.01). Compared with the experimental group, Scr (63.88±2.01) μmol/L, Bun (5.45±0.47) mmol/L, paller score (4.8±0.2), IL-1β (78.61±3.66) pg/mL, IL-6 (297.90±13.64) pg/mL and TNF-α (276.2±20.18) pg/mL were significantly decreased in the levosimendan group (all P<0.01). TUNEL staining showed that levosimendan could improve the apoptosis of renal cells ( P<0.01). The expression of p-ERK protein in the levosimendan group was significantly higher than that in the experimental group ( P<0.01). Conclusions:Lovosimendan could attenuate acute kidney injury following cardiac arrest and cardiopulmonary resuscitation via suppression apoptosis. The mechanism of levosimendan protective effect might be associated with activation of ERK signaling pathway.

Objective:To evaluate the effects of mouse nerve growth factor (mNGF) on the brain water content and the expressions of β-amyloid precursor protein (β-APP) and neurofilament light polypeptide (NF-L) in rats with traumatic brain injury (TBI) complicated by seawater drowning (SWD). Methods:A total of 60 male rats were randomly divided into three groups: Sham group ( n=12), TBI+ SWD group ( n=24), and mNGF group ( n=24). The rat models were created on the basis of Marmarou′s weight-drop TBI modeling and instilling seawater into the trachea by syringe pump. The mNGF group was administered mNGF intraperitoneally; while the Sham group and the TBI+ SWD group were injected with an equivalent amount of normal saline. The brain water content was measured by using the dry-wet weight method. The pathological changes of the hippocampal tissue and the expressions of β-APP and NF-L were observed through hematoxylin-eosin (HE) staining and immunohistochemical (IHC) staining. Results:Brain water content in the mNGF group was similar to that in the TBI+ SWD group ( P>0.05). Compared with the TBI+ SWD group, the expressions of β-APP and NF-L in the hippocampal tissue of the mNGF group were significantly reduced. Conclusion:mNGF can reduce the expressions of β-APP and NF-L, and protect the neurons of the rats after TBI+ SWD.

Objective:To evaluate the effects of mouse nerve growth factor (mNGF) on the brain water content and the expressions of β-amyloid precursor protein (β-APP) and neurofilament light polypeptide (NF-L) in rats with traumatic brain injury (TBI) complicated by seawater drowning (SWD). Methods:A total of 60 male rats were randomly divided into three groups: Sham group ( n=12), TBI+ SWD group ( n=24), and mNGF group ( n=24). The rat models were created on the basis of Marmarou′s weight-drop TBI modeling and instilling seawater into the trachea by syringe pump. The mNGF group was administered mNGF intraperitoneally; while the Sham group and the TBI+ SWD group were injected with an equivalent amount of normal saline. The brain water content was measured by using the dry-wet weight method. The pathological changes of the hippocampal tissue and the expressions of β-APP and NF-L were observed through hematoxylin-eosin (HE) staining and immunohistochemical (IHC) staining. Results:Brain water content in the mNGF group was similar to that in the TBI+ SWD group ( P>0.05). Compared with the TBI+ SWD group, the expressions of β-APP and NF-L in the hippocampal tissue of the mNGF group were significantly reduced. Conclusion:mNGF can reduce the expressions of β-APP and NF-L, and protect the neurons of the rats after TBI+ SWD.

Objective To explore the role of TLR4/NF-kB signal pathway in rat nerve injury after traumatic brain injury coupled with seawater drowning.Methods A total of 96 male Sprague-Dawley rats were randomly divided into 3 groups:the sham surgery group(n =12),the traumatic brain injury (TBI) group(n =42) and the traumatic brain injury coupled with seawater drowning group (or the TBI + SWD group) (n =42).At the timepoints of 3,6,12,24,72 and 168 hours after the establishment of the TBI model,immunohistochemistry was used to detect the expression of TLR4 and NF-kB cells in the rat brain tissue.Real time PCR (rt-PCR) was applied to detect the expression levels of TLR4 and NF-kB mRNA in the hippocampus of the brain tissue,and enzyme-linked immunosorbent assay (ELISA) was employed to detect the content of TNF-α in the rat brain tissue.Results The number of TLR4 and NF-kB positive cells in the brain tissue of the TBI group and the TBI + searwater drowning group increased.The expressions of TLR4 and NF-kB mRNA in the hippocampus of the brain tissue of the TBI group and the TBI + SWD group significantly increased 3 hours after establishment of the TBI model.For the TBI group,the expressions of TLR4 and NF-kB were respectively (1.63 ±0.52) and (1.52 ±0.41),while in the the TBI + SWD group,the expressions of the above 2 substantce were respectively (4 1.87 ± 0.93) and (1.87 ± 0.93).At hour 24,the expression reached peak.For the TBI group,the expressions of TLR4 and NF-kB were respectively (49.61 ± 0.34) and (4.60 ± 0.51),while for the the TBI + SWD group,the expressions of the above 2 substantces were respectively (16.11 ±0.49) and (5.80 ± 0.52),then they decreased gradually.The expression levels of TNF-α in the TBI group and the TBI + SWD group were found to elevate 3 hours after establishment of the model.TNF-α expression level for the TBI group was (53.68 ± 1.48) ng/L),while the expression level of the same substance for the TBI + SWD group was (60.14 ± 2.06) ng/L.Wave peak appeared at hour 12,and the wave peak for the TBI group was (79.28 ± 2.46) ng/L,while for the TBI + SWD group,it displayed at (103.51 ± 5.53) ng/L.Conclusion Seawater drowning could aggravate nerve inflammatory response mediated by TLR4/NF-kB signal pathway,which might play an important role in the rat brain injury induced by trauma.

Objective To establish an animal model of traumatic brain injury coupled with acute lung injury induced by seawater drowning.Methods A total of 80 male Sprague-Dawley rats were randomly divided into 4 groups:the sham group,the traumatic brain injury (TBI) group,the seawater drowning-induced acute lung injury (SWD-ALI) group and the traumatic brain injury coupled with seawater drowning-induced acute lung injury (TBI + SWD-ALI) group,each consisting of 20 animals.The TBI model group was established with the impact power of 450 g × 1.5 m by the " Marmarou method".The SWD-ALI group was established by pumping the artificial seawater into the rat trachea at a rate of 3 ml/kg.The TBI + SWD-ALI group was established on the basis of TBI.The data of arterial blood gases were detected 10,30,60,120 and 240 minutes after trauma injury.Wet/dry weight of the lung was detected 240min after injury,and pulmonary pathological changes were also observed after HE staining.Pathological changes in the brain tissue after HE staining and the expression levels of/3-APP and NF-L after immunohistochemical (IHC) staining were observed 24 hours after injury.Results The levels of PaO2 after injury during observation period generally displayed an increasing trend in the TBI,the SWD-ALI and the TBI + SWD-ALI groups.The levels of PaO2 10 minutes after injury were the lowest,which were respectively (85.12 ± 2.03) mmHg,(37.75 ± 1.17) mmHg and (33.38 ± 1.92) mmHg,and were obviously lower than that of the sham group (95.25 ± 2.05) mmHg,with statistical significance (P＜0.05).The levels of PaO2 at the time point of 240 minutes after injury reached peak,which were respectively (96.63 ± 1.60) mmHg,(86.13 ± 2.03) mmHg and (77.25 ± 3.33) mmHg,and the levels of PaO2 for the SWD-ALI and TBI + SWD-ALI groups were significantly lower than that of the sham group [(97.50 ± 1.20) mmHg],also with statistical significance (P ＜ 0.05).The levels of PaO2 in the TBI + SWD-ALI group was considerably lower than that of the SWD-ALI group (P ＜ 0.05).The ratios of wet/ dry weight of the lung tissue at the time point of 240 minutes after injury for the SWD-ALI group and the TBI + SWD-ALI group were respectively (7.30 ± 0.16) and (7.34 ± 0.21),which were all obviously higher than those of the sham group (4.81 ±0.18) and the TBI group (4.91 ±0.18),also with statistical significance (P ＜ 0.05).However,no statistical significance could be seen,when comparisons were made between the SWD-ALI and TBI + SWD-ALI groups (P ＞ 0.05).HE staining indicated that such pulmonary pathological lesions as wider alveolar septa,alveolar space fusion,inflammatory cell infiltration in various degrees could be observed in the SWD-ALI and TBI + SWD-ALI groups.In addition,brain tissue HE staining revealed that neuronal cell degeneration in the cortex of the brain tissue could be detected in the TBI,SWD-ALI and TBI + SWD-ALI groups,and immunohistochemical staining indicated that there were positive expressions of β-APP and NF-L in the TBI and TBI + SWD-ALI groups.Conclusion The impact with the power of 450 g × 1.5 m by the "the Marmarou method" followed by pumping of seawater (3 ml/kg) into trachea could establish a stable and reproductive rat model of traumatic brain injury coupled with acute lung injury induced by seawater drowning.

Objective To explore the role of TLR4/NF-kB signal pathway in rat nerve injury after traumatic brain injury coupled with seawater drowning.Methods A total of 96 male Sprague-Dawley rats were randomly divided into 3 groups:the sham surgery group(n =12),the traumatic brain injury (TBI) group(n =42) and the traumatic brain injury coupled with seawater drowning group (or the TBI + SWD group) (n =42).At the timepoints of 3,6,12,24,72 and 168 hours after the establishment of the TBI model,immunohistochemistry was used to detect the expression of TLR4 and NF-kB cells in the rat brain tissue.Real time PCR (rt-PCR) was applied to detect the expression levels of TLR4 and NF-kB mRNA in the hippocampus of the brain tissue,and enzyme-linked immunosorbent assay (ELISA) was employed to detect the content of TNF-α in the rat brain tissue.Results The number of TLR4 and NF-kB positive cells in the brain tissue of the TBI group and the TBI + searwater drowning group increased.The expressions of TLR4 and NF-kB mRNA in the hippocampus of the brain tissue of the TBI group and the TBI + SWD group significantly increased 3 hours after establishment of the TBI model.For the TBI group,the expressions of TLR4 and NF-kB were respectively (1.63 ±0.52) and (1.52 ±0.41),while in the the TBI + SWD group,the expressions of the above 2 substantce were respectively (4 1.87 ± 0.93) and (1.87 ± 0.93).At hour 24,the expression reached peak.For the TBI group,the expressions of TLR4 and NF-kB were respectively (49.61 ± 0.34) and (4.60 ± 0.51),while for the the TBI + SWD group,the expressions of the above 2 substantces were respectively (16.11 ±0.49) and (5.80 ± 0.52),then they decreased gradually.The expression levels of TNF-α in the TBI group and the TBI + SWD group were found to elevate 3 hours after establishment of the model.TNF-α expression level for the TBI group was (53.68 ± 1.48) ng/L),while the expression level of the same substance for the TBI + SWD group was (60.14 ± 2.06) ng/L.Wave peak appeared at hour 12,and the wave peak for the TBI group was (79.28 ± 2.46) ng/L,while for the TBI + SWD group,it displayed at (103.51 ± 5.53) ng/L.Conclusion Seawater drowning could aggravate nerve inflammatory response mediated by TLR4/NF-kB signal pathway,which might play an important role in the rat brain injury induced by trauma.

Objective To establish an animal model of traumatic brain injury coupled with acute lung injury induced by seawater drowning.Methods A total of 80 male Sprague-Dawley rats were randomly divided into 4 groups:the sham group,the traumatic brain injury (TBI) group,the seawater drowning-induced acute lung injury (SWD-ALI) group and the traumatic brain injury coupled with seawater drowning-induced acute lung injury (TBI + SWD-ALI) group,each consisting of 20 animals.The TBI model group was established with the impact power of 450 g × 1.5 m by the " Marmarou method".The SWD-ALI group was established by pumping the artificial seawater into the rat trachea at a rate of 3 ml/kg.The TBI + SWD-ALI group was established on the basis of TBI.The data of arterial blood gases were detected 10,30,60,120 and 240 minutes after trauma injury.Wet/dry weight of the lung was detected 240min after injury,and pulmonary pathological changes were also observed after HE staining.Pathological changes in the brain tissue after HE staining and the expression levels of/3-APP and NF-L after immunohistochemical (IHC) staining were observed 24 hours after injury.Results The levels of PaO2 after injury during observation period generally displayed an increasing trend in the TBI,the SWD-ALI and the TBI + SWD-ALI groups.The levels of PaO2 10 minutes after injury were the lowest,which were respectively (85.12 ± 2.03) mmHg,(37.75 ± 1.17) mmHg and (33.38 ± 1.92) mmHg,and were obviously lower than that of the sham group (95.25 ± 2.05) mmHg,with statistical significance (P＜0.05).The levels of PaO2 at the time point of 240 minutes after injury reached peak,which were respectively (96.63 ± 1.60) mmHg,(86.13 ± 2.03) mmHg and (77.25 ± 3.33) mmHg,and the levels of PaO2 for the SWD-ALI and TBI + SWD-ALI groups were significantly lower than that of the sham group [(97.50 ± 1.20) mmHg],also with statistical significance (P ＜ 0.05).The levels of PaO2 in the TBI + SWD-ALI group was considerably lower than that of the SWD-ALI group (P ＜ 0.05).The ratios of wet/ dry weight of the lung tissue at the time point of 240 minutes after injury for the SWD-ALI group and the TBI + SWD-ALI group were respectively (7.30 ± 0.16) and (7.34 ± 0.21),which were all obviously higher than those of the sham group (4.81 ±0.18) and the TBI group (4.91 ±0.18),also with statistical significance (P ＜ 0.05).However,no statistical significance could be seen,when comparisons were made between the SWD-ALI and TBI + SWD-ALI groups (P ＞ 0.05).HE staining indicated that such pulmonary pathological lesions as wider alveolar septa,alveolar space fusion,inflammatory cell infiltration in various degrees could be observed in the SWD-ALI and TBI + SWD-ALI groups.In addition,brain tissue HE staining revealed that neuronal cell degeneration in the cortex of the brain tissue could be detected in the TBI,SWD-ALI and TBI + SWD-ALI groups,and immunohistochemical staining indicated that there were positive expressions of β-APP and NF-L in the TBI and TBI + SWD-ALI groups.Conclusion The impact with the power of 450 g × 1.5 m by the "the Marmarou method" followed by pumping of seawater (3 ml/kg) into trachea could establish a stable and reproductive rat model of traumatic brain injury coupled with acute lung injury induced by seawater drowning.