Objective:To construct an effectiveness evaluation model of internal control of medical equipment in public hospitals based on fuzzy analytic network process(F-ANP),and to improve the level of internal control management of medical equipment in hospitals.Methods:Through literature research and analysis,based on the internal control theory system of The Committee of Sponsoring Organizations of the Treadway Commission(COSO),combined with the characteristics of medical equipment management in public hospitals,the effectiveness evaluation model of internal control of medical equipment in public hospitals was established by F-ANP,which was combining analytic network process(ANP)and fuzzy comprehensive evaluation.An empirical analysis was carried out on the internal control of medical equipment in Beijing Friendship Hospital,Capital Medical University.Results:The index system for model evaluation included 5 first-level indicators of control environment,risk evaluation,control activities,information exchange,and supervision mechanism,17 second-level indicators,and 50 third-level indicators.The model was used to evaluate the effectiveness of internal control of medical equipment in the hospital,its maximum membership value was 0.133 7,and the result was"relatively effective",indicating that the construction and implementation of internal control of medical equipment in the hospital were relatively perfect,while the management of scrapping of medical equipment,cost control and equipment informatization construction still need to be improved.Conclusion:The effectiveness evaluation model of internal control of medical equipment of public hospitals based on F-ANP can provide certain reference value for evaluation of the effectiveness of internal control of medical equipment in public hospitals,which is conducive to standardizing internal control of medical equipment,promoting the fine management of medical equipment and ensuring the safety of medical equipment assets.

Hypertrophic scar is an abnormal fibrous proliferative disease that occurs after deep cutaneous injury, which not only affects aesthetics and function but also has negative psychological effects on the patients. However, the mechanism of hypertrophic scar formation has not been fully elucidated, and its clinical treatment is complex with a high rate of recurrence and no radicle cure. Intervention based on molecular targets will likely be the future direction for the prevention and treatment of hypertrophic scar. In this article, we review the specific roles and mechanisms of drug-targeted interventions in hypertrophic scar formation, including general drugs, cytokines, immunomodulators, herbal extracts, exosomes, and nanomaterials, in the context of advances in both basic and clinical research at home and abroad.

Acute lung injury/acute respiratory distress syndrome (ALI/ARDS) is a respiratory disorder with high morbidity and mortality caused by various causes. Exosomes can mediate cell communication through paracrine pathways, transfer proteins, lipids, nucleic acids, etc., and interfere with the biological functions of recipient cells. Various cell-derived exosomes have been reported to play an immunomodulatory role in the ALI/ARDS inflammatory model. This article reviews the mechanism of exosomes involved in immune regulation of ALI/ARDS and possible therapeutic approaches.

Objective:To assess the prognostic value of modified Charlson comorbidity index (mCCI) combined with serum albumin for long-term prognosis in peritoneal dialysis (PD) patients.Methods:From January 1, 2007 to June 30, 2015, patients who started PD in Nanjing Drum Tower Hospital were enrolled in this retrospective cohort study. Clinical data including gender, age, underlying diseases, laboratory examination and prognosis were collected. The mCCI at the beginning of PD was calculated. Whether the duration of PD exceeded 5 years was used as an indicator to evaluate the prognosis. The patients were divided into≥5 years group and<5 years group according to the duration of PD, and the data were compared between the two groups. Cox regression model was constructed to analyze the influencing factors of all-cause death in PD patients. Multivariate logistic regression model and receiver operating characteristic (ROC) curve were used to analyze the predictive value of mCCI and serum albumin levels on whether patients could maintain long-term PD.Results:Of the 183 patients included [males 106(57.9%), females 77(42.1%); (53.35±16.50) years old; 162 cases (88.5%) with hypertension, 55 cases (30.1%) with diabetes], 97 cases had PD duration for ≥5 years and 86 cases less than 5 years. The overall 5-year technical survival rate was 65.1%. At the beginning of PD, compared with the dialysis age≥5 years group, the patients in the dialysis age less than 5 years group had older age, higher mCCI, lower serum albumin level, and higher C-reactive protein (CRP) level (all P<0.05), but there were no significant differences in gender, education level, electrolyte, mean arterial pressure, high densitv lipoprotein (HDL), low-density lipoprotein (LDL) and PD adequacy index between the two groups (all P>0.05). Multivariate logistic regression analysis showed that increased age ( OR=1.022, 95% CI 1.000-1.043, P=0.046), increased mCCI ( OR=1.620, 95% CI 1.300-2.018, P<0.001) and decreased serum albumin ( OR=0.807, 95% CI 0.730-0.893, P<0.001) were independent predictors for the duration of PD<5 years. ROC curve analysis showed that the area under ROC curves ( AUC) of mCCI, serum albumin level and combined prediction probability of the two for the duration of PD<5 years were 0.647(95% CI 0.568-0.727), 0.655(95% CI 0.577-0.734), and 0.767(95% CI 0.700-0.835), respectively, indicating that the accuracy of combined parameters to predict survival outcome was higher than that of any single parameter. Multivariate Cox analysis showed that increased age ( HR=1.073, 95% CI 1.046-1.100, P<0.001), increased mCCI ( HR=1.198, 95% CI 1.044-1.375, P=0.010) and decreased serum albumin ( HR=0.904, 95% CI 0.843-0.969, P=0.004) were independent influencing factors for all-cause death in PD patients. Conclusions:Old age, high mCCI and low serum albumin level are influencing factors for dialysis age<5 years and all-cause death in PD patients. mCCI combined with serum albumin level can improve the accuracy of predicting the long-term dialysis in PD patients.

Objective:To explore the fluid resuscitation strategy in shock stage in severely burned children with different burn areas in different age groups, and to evaluate the curative effect.Methods:A retrospective cohort study was conducted. From January 2015 to June 2020, 235 children with severe and above burns who met the inclusion criteria were hospitalized in the First Affiliated Hospital of Nanchang University, including 150 males and 85 females, aged 3 months to 12 years. After admission, it was planned to rehydrate the children with electrolyte, colloid, and water according to the domestic rehydration formula for pediatric burn shock, and the rehydration volume and speed were adjusted according to the children's mental state, peripheral circulation, heart rate, blood pressure, and urine output, etc. The actual input volume and planned input volume of electrolyte, colloid, water, and total fluid of all the children were recorded during the 8 hours since fluid replacement and the first and second 24 hours after injury. According to urine output during the 8 hours since fluid replacement, all the children were divided into satisfactory urine output maintenance group (119 cases) with urine output ≥1 mL·kg -1·h -1 and unsatisfactory urine output maintenance group (116 cases) with urine output <1 mL·kg -1·h -1, and the electrolyte coefficient, colloid coefficient, and water coefficient of the children were calculated during the 8 hours since fluid replacement. According to the total burn area, children aged <3 years (155 cases) and 3-12 years (80 cases) were divided into 15%-25% total body surface area (TBSA) group and >25%TBSA group, respectively. The electrolyte coefficient, colloid coefficient, water coefficient, and urine output of the children were calculated or counted during the first and second 24 hours after injury, and the non-invasive monitoring indicators of body temperature, heart rate, respiratory rate, and percutaneous arterial oxygen saturation and efficacy indicators of hematocrit, platelet count, hemoglobin, albumin, creatinine, and alanine aminotransferase (ALT) of the children were recorded 48 hours after injury. The prognosis and outcome indicators of all the children during the treatment were counted, including complications, cure, improvement and discharge, automatic discharge, and death. Data were statistically analyzed with independent sample or paired sample t test, Mann-Whitney U test, chi-square test, and Fisher's exact probability test. Results:During the 8 hours since fluid replacement, the actual input volume of electrolyte of all the children was significantly more than the planned input volume, and the actual input volumes of colloid, water, and total fluid were significantly less than the planned input volumes ( Z=13.094, 5.096, 13.256, 7.742, P<0.01). During the first and second 24 hours after injury, the actual input volumes of electrolyte of all the children were significantly more than the planned input volumes, and the actual input volumes of water and total fluid were significantly less than the planned input volumes ( Z=13.288, -13.252, 3.867, 13.183, -13.191, 10.091, P<0.01), while the actual input volumes of colloid were close to the planned input volumes ( P>0.05). During the 8 hours since fluid replacement, compared with those in unsatisfactory urine output maintenance group, there was no significant change in electrolyte coefficient or colloid coefficient of children in satisfactory urine output maintenance group ( P>0.05), while the water coefficient was significantly increased ( Z=2.574, P<0.05). Among children <3 years old, compared with those in >25%TBSA group, the electrolyte coefficient and water coefficient of children were significantly increased and the urine output of children was significantly decreased in 15%-25%TBSA group during the first and second 24 hours after injury ( Z=-3.867, -6.993, -3.417, -5.396, -5.062, 1.503, P<0.05 or P<0.01), while the colloid coefficient did not change significantly ( P>0.05); the levels of efficacy indicators of hematocrit, platelet count, and hemoglobin at 48 h after injury were significantly increased, while ALT level was significantly decreased ( Z=-2.720, -3.099, -2.063, -2.481, P<0.05 or P<0.01); the levels of the rest of the efficacy indicators and non-invasive monitoring indicators at 48 h after injury did not change significantly ( P>0.05). Among children aged 3-12 years, compared with those in >25%TBSA group, the electrolyte coefficient and water coefficient of children in 15%-25%TBSA group were significantly increased during the first and second 24 hours after injury, the colloid coefficient during the second 24 h was significantly decreased ( Z=-2.042, -4.884, -2.297, -3.448, -2.480, P<0.05 or P<0.01), while the colloid coefficient during the first 24 hours after injury, urine output during the first and second 24 hours after injury, and the non-invasive monitoring indicators and efficacy indicators at 48 hours after injury did not change significantly ( P>0.05). Complications occurred in 17 children during the treatment. Among the 235 children, 211 cases were cured, accounting for 89.79%, 5 cases were improved and discharged, accounting for 2.13%, 16 cases were discharged automatically, accounting for 6.81%, and 3 cases died, accounting for 1.28%. Conclusions:The electrolyte volume in early fluid resuscitation in severely burned children exceeding the volume calculated by the formula can obtain a good therapeutic effect. Among children <3 years old, the volume of fluid resuscitation should be appropriately increased in children with extremely severe burns compared with children with severe burns during fluid resuscitation; among children aged 3-12 years, the colloid volume should be appropriately increased in children with extremely severe burns compared with children with severe burns during fluid resuscitation; non-invasive monitoring indicators can be used to monitor hemodynamics and guide fluid resuscitation in severely burned children.

As one of the important means for saving severely burned patients, mechanical ventilation can not only improve the function of important organs such as heart, lung, and kidney, but also stabilize the homeostasis of the body, thus promoting the recovery of patients. Improper use of mechanical ventilation, however, can lead to many complications, among which the ventilator-induced lung injury (VILI) is one of the most common and serious complications, accompanying with a high mortality rate. The target of preventing VILI is to minimize the risk of lung injury caused by mechanical ventilation. This article reviews the pathogenesis, diagnosis, and early prevention and treatment of VILI caused by mechanical ventilation in burned patients.

Objective:To explore the mechanism of 14-3-3σgene in regulating inflammatory response of human pulmonary epithelial cells induced by endotoxin/lipopolysaccharide (LPS).Methods:(1) Cells of human normal pulmonary epithelial cell line BEAS-2B cultured in logarithmic growth period were collected and divided into control group and PCMV6-14-3-3σgroup using the random number table, with 3 wells in each group. Cells in control group were transfected with empty plasmid, and cells in PCMV6-14-3-3σgroup were transfected with PCMV6-14-3-3σplasmid. The protein expression of 14-3-3σin cell was detected by Western blotting at 48 hours after transfection. (2) Cells of human normal pulmonary epithelial cell line BEAS-2B cultured in logarithmic growth period were collected and divided into control group, PCMV6-14-3-3σgroup, PCMV6-14-3-3σ+ LPS group, and LPS group using the random number table, with 3 wells in each group. Cells in control group were transfected with empty plasmid for 42 hours. Cells in PCMV6-14-3-3σgroup were transfected with PCMV6-14-3-3σplasmid for 42 hours. Cells in PCMV6-14-3-3σ+ LPS group were stimulated with 1 μg/mL LPS (the same final mass concentration below) for 6 hours after being transfected with PCMV6-14-3-3σplasmid for 42 hours. Cells in LPS group were stimulated by LPS for 6 hours. The protein expressions of Bax and B-cell lymphoma-2 (Bcl-2) were detected by Western blotting, and the ratio of Bax to Bcl-2 was calculated. Apoptotic rate was detected by flow cytometry. The mRNA expressions of tumor necrosis factor alpha (TNF-α) and interleukin 1beta (IL-1β) in cells were detected by real-time fluorescent quantitative reverse transcription polymerase chain reaction technique. Content of TNF-α and IL-1β in cell culture supernatant was detected by enzyme-linked immunosorbent assay. Data were statistically analyzed with t test, one-way analysis of variance, and least significant difference test. Results:(1) At 48 hours after transfection, the protein expression of 14-3-3σin cells of PCMV6-14-3-3σgroup (1.05±0.03) was significantly higher than that in control group (0.78±0.04, t=5.41, P<0.01). (2) Compared with those in control group, the ratio of Bax to Bcl-2, apoptotic rate, mRNA expressions of TNF-α and IL-1β, and content of TNF-α and IL-1β in cell supernatant in PCMV6-14-3-3σgroup showed no significant difference ( P>0.05); the above-mentioned indexes of cells in LPS group were significantly higher or increased ( P<0.01). Compared with those in LPS group, the above-mentioned indexes of cells in PCMV6-14-3-3σ+ LPS group were significantly lower or decreased ( P<0.01). Conclusions:14-3-3σis a key factor in regulating apoptosis. It can alleviate the LPS-induced inflammatory responses by regulating the ratio of apoptotic regulators Bax to Bcl-2 and inhibiting apoptosis of human pulmonary epithelial cells.

Objective: To investigate the effect of recombinant human keratinocyte growth factor 2 (rhKGF-2) on lung tissue of rabbits with severe smoke inhalation injury. Methods: A total of 120 New Zealand rabbits were divided into 5 groups by random number table after being inflicted with severe smoke inhalation injury, with 24 rats in each group. Rabbits in the simple injury group inhaled air, while rabbits in the injury+phosphate buffer solution (PBS) group inhaled 5 mL PBS once daily for 7 d. Rabbits in injury+1 mg/kg rhKGF-2 group, injury+2 mg/kg rhKGF-2 group, and injury+5 mg/kg rhKGF-2 group received aerosol inhalation of 1 mg/kg, 2 mg/kg, and 5 mg/kg rhKGF-2 (all dissolved in 5 mL PBS) once daily for 7 d, respectively. On treatment day 1, 3, 5, and 7, blood samples were taken from the ear central artery of 6 rabbits in each group. After the blood was taken, the rabbits were sacrificed, and the tracheal carina tissue and lung were collected. Blood pH value, arterial oxygen partial pressure (PaO₂), arterial blood carbon dioxide pressure (PaCO₂), and bicarbonate ion were detected by handheld blood analyzer. The expressions of pulmonary surfactant-associated protein A (SP-A) and vascular endothelial growth factor (VEGF) in lung tissue were detected by Western blotting. Pathomorphology of lung tissue and trachea was observed by hematoxylin-eosin staining. Data were processed with analysis of variance of two-way factorial design and Tukey test. Results: (1) Compared with those in simple injury group, the blood pH values of rabbits in the latter groups on treatment day 1-7 had no obvious change (P>0.05). The PaO₂ of rabbits in injury+2 mg/kg rhKGF-2 group on treatment day 5 and 7 were (75.0±2.4) and (71.0±4.5) mmHg (1 mmHg=0.133 kPa), respectively, which were significantly higher than (62.0±6.8) and (63.0±3.0) mmHg in simple injury group (q=4.265, 8.202, P<0.05 or P<0.01). The PaO₂ of rabbits in injury+5 mg/kg rhKGF-2 group on treatment day 7 was (82.0±4.9) mmHg, which was significantly higher than that in simple injury group (q=6.234, P<0.01). Compared with that in simple injury group, the PaCO₂ of rabbits in injury+2 mg/kg rhKGF-2 group on treatment day 3 was significantly decreased (q=4.876, P<0.01) and significantly increased on treatment day 5 (q=5.562, P<0.01); the PaCO₂ of rabbits in injury+5 mg/kg rhKGF-2 group was significantly increased on treatment day 5 and 7 (q=5.013, 4.601, P<0.05 or P<0.01). Compared with that in simple injury group, the serum bicarbonate ion of rabbits in injury+1 mg/kg rhKGF-2 group on treatment day 7 was significantly increased (q=5.142, P<0.01); the serum bicarbonate ion of rabbits in injury+2 mg/kg rhKGF-2 group on treatment day 5 and 7 were significantly increased (q=4.830, 6.934, P<0.01); the serum bicarbonate ion of rabbits in injury+5 mg/kg rhKGF-2 group on treatment day 5 were significantly increased (q=3.973, P<0.05). (2) The expressions of SP-A in lung tissue of rabbits in simple injury group and injury+PBS group in each treatment time point were close (P>0.05). The expressions of SP-A in lung tissue of rabbits in injury+2 mg/kg rhKGF-2 group and injury+5 mg/kg rhKGF-2 group on treatment day 3 were 0.091±0.007 and 0.101±0.009, respectively, significantly higher than 0.069±0.009 in simple injury group (q=10.800, 13.580, P<0.01). The expressions of SP-A in lung tissue of rabbits in injury+1 mg/kg rhKGF-2 group, injury+2 mg/kg rhKGF-2 group, and injury+5 mg/kg rhKGF-2 group on treatment day 5 and 7 were 0.127±0.008, 0.132±0.006, 0.194±0.006, 0.152±0.017, 0.166±0.004, 0.240±0.008, significantly higher than 0.092±0.003 and 0.108±0.005 in simple injury group (q=6.789, 12.340, 17.900, 9.875, 31.480, 40.740, P<0.01). (3) On treatment day 1 and 5, there was no significant difference in the expression of VEGF in lung tissue of rabbits among the 5 groups (P>0.05). Compared with those in simple injury group, the expressions of VEGF in lung tissue of rabbits in injury+2 mg/kg rhKGF-2 group on treatment day 3 and 7 were significantly increased (q=4.243, 8.000, P<0.05 or P<0.01), and the expression of VEGF in lung tissue of rabbits in injury+5 mg/kg rhKGF-2 group on treatment day 7 was significantly increased (q=20.720, P<0.01). (4) On treatment day 1, the injury of rabbits in each group was similar, with a large number of neutrophils infiltrated and abscess formed in the alveolar and interstitial tissue, thickened alveolar septum, some collapsed alveolar and atelectasis; large area of tracheal mucosa was degenerated and necrotic, with a large amount of inflammatory exudates blocking in the cavity. On treatment day 3, the inflammation of lung tissue and trachea in each group were improved, but the inflammation in simple injury group and injury+PBS group was also serious. On treatment day 5, the inflammation in lung tissue and trachea of rabbits in injury+2 mg/kg rhKGF-2 group and injury+5 mg/kg rhKGF-2 group were improved much obviously than those in the other groups. On treatment day 7, the inflammation in lung tissue of rabbits in injury+5 mg/kg rhKGF-2 group alleviated obviously than those in the other groups, most alveoli had no obvious exudative fluid, the alveolar cavity was intact and clear, the local alveolar dilated like a cyst, and the alveolar septum thinning; the improvement of inflammation of trachea was more obvious than the other groups, the tracheal mucosa tended to be more complete, and few neutrophils were infiltrated in the endotracheal cavity. Conclusions Atomization inhalation of rhKGF-2 can improve the PaO₂ level of rabbits with severe smoke inhalation injury, reduce airway inflammation, increase the expression of SP-A and VEGF in lung tissue, thus promoting the repair of lung tissue.

Acute lung injury (ALI) is a clinically common critical disease with various treatment methods. Stem cell has drawn great attention for excellent performance in treatment of ALI. However, due to its high apoptosis rate, the further clinical application of stem cell is restricted. Exosomes are a kind of extracellular vesicles secreted by cells, which play important role in injury repair with further research about exosomes. This article reviews current situation, brief introduction to exosomes, repair effects of exosomes on ALI, and the potential signal pathway.

Objective: To investigate the effects of non-muscle myosin ⅡA (NMⅡA) silenced bone marrow mesenchymal stem cells (BMSCs) on the lung damage of rats at early stage of smoke inhalation injury. Methods: Forty Sprague-Dawley rats were divided into control, simple injury, NMⅡA-BMSCs, and BMSCs groups according to the completely random method, with 10 rats in each group. Rats in control group inhaled air normally, while rats in the latter 3 groups inhaled smoke to reproduce model of smoke inhalation injury. At 30 min post injury, rats in simple injury group were injected with 1 mL normal saline via caudal vein, and rats in group BMSCs were injected with 1 mL the fifth passage of BMSCs (1×10⁷/mL), and rats in group NMⅡA-BMSCs were injected with 1 mL NMⅡA silenced BMSCs (1×10⁷/mL). At post injury hour (PIH) 24, abdominal aorta blood and right lung of rats in each group were harvested, and then arterial partial pressure of oxygen (PaO₂), arterial partial pressure of carbon dioxide (PaCO₂), and pH value were detected by blood gas analyzer. Ratio of wet to dry weight of lung was determined by dry-wet weight method. Pathological changes of lung were observed with HE staining. Bronchoalveolar lavage fluid (BALF) were collected, and then tumor necrotic factor-α (TNF-α) and interleukin-10 (IL-10) content of BALF was determined by enzyme-linked immunosorbent assay. Data were processed with one-way analysis of variance, Kruskal-Wallis H test, and least-significant difference test. Results: (1) At PIH 24, compared with those in control group, PaO₂ values of rats in simple injury, BMSCs, and NMⅡA-BMSCs groups were obviously decreased (with P values below 0.05), and PaCO₂ values were obviously increased (with P values below 0.05). Compared with those in simple injury group, PaO₂ values of rats in groups NMⅡA-BMSCs and BMSCs were obviously increased (with P values below 0.05), while PaCO₂ values were obviously decreased (with P values below 0.05). PaO₂ value of rats in group NMⅡA-BMSCs was obviously increased as compared with that in group BMSCs (P<0.05). The pH value of arterial blood of rats in simple injury group was obviously lower than that in control group (P<0.05). (2) At PIH 24, ratios of wet to dry weight of lung of rats in control, simple injury, BMSCs, and NMⅡA-BMSCs groups were 4.36±0.15, 7.79±0.42, 5.77±0.18, and 5.11±0.20, respectively. Compared with that in control group, ratio of wet to dry weight of lung of rats was obviously increased in the other 3 groups (with P values below 0.05). Compared with that in simple injury group, ratio of wet to dry weight of lung of rats was obviously decreased in groups BMSCs and NMⅡA-BMSCs (with P values below 0.05). Compared with that in group BMSCs, ratio of wet to dry weight of lung of rats in group NMⅡA-BMSCs was obviously decreased (P<0.05). (3) At PIH 24, alveolar structure of rats in control group was complete without abnormality. Compared with those in simple injury group, lung injury and infiltration of inflammatory cells of rats in groups BMSCs and NMⅡA-BMSCs were obviously alleviated, and alveolar structure was relatively complete with no thickening of alveolar wall. (4) At PIH 24, compared with that in control group, TNF-α content of BALF of rats in simple injury and BMSCs groups was obviously increased (with P values below 0.05). Compared with that in simple injury group, TNF-α content of BALF in groups BMSCs and NMⅡA-BMSCs was obviously decreased (with P values below 0.05). Compared with that in control group, IL-10 content of BALF in simple injury, NMⅡA-BMSCs and BMSCs groups were obviously increased (with P values below 0.05). Compared with that in simple injury group, IL-10 content of BALF in groups BMSCs and NMⅡA-BMSCs was obviously increased (with P values below 0.05). Compared with that in group BMSCs, IL-10 content of BALF in group NMⅡA-BMSCs was obviously increased (P<0.05). Conclusions NMⅡA silenced BMSCs can alleviate lung damage of rats at early stage of smoke inhalation injury, showing better effectiveness than using BMSCs only.