Objective To investigate the potential roles of nucleotide -binding oligomerization domain (NOD)-like receptor in the pathogenesis of asthma.Methods Through rat asthma model,24 rats were randomly divided into three groups on average,named asthma group,control group and dexamethasone group.Expression levels of NOD1 and NOD2 mRNA were detected by Real -time PCR in lung tissues.Results The expression levels of NOD1 mRNA in the asthma group,control group and dexamethasone group were (0.62 ±0.34)RQ value,(1 .00 ± 0.00)RQ value,(0.65 ±0.33 )RQ value respectively.The levels of NOD1 mRNA in the asthma group was significantly lower than that in the control group(F =4.75,P <0.05 ),while there was no statistically significant difference of NOD1 mRNA level between the dexamethasone group and asthma group(P >0.05).Moreover,expression levels of NOD2 mRNA in the asthma group,control group and dexamethasone group were (0.92 ±0.32)RQ value, (1 .00 ±0.00)RQ value,(1 .50 ±0.56)RQ value,respectively.There was no statistically significant difference of NOD2 mRNA level between the asthma group and control group (P >0.05 ),but level of NOD2 mRNA in the dexamethasone group was significantly higher than that in the asthma group(F =5.64,P <0.01 ).And there was no significant correlation between level of NOD1 and NOD2 mRNA(r =0.1 5,P >0.05).Conclusion Expression of NOD -like receptor subtype was not at the same level,and their reaction to dexamethasone were different either.

Objective To observe the effects of dexmedetomidine for different loading dose on blood pressure of surgery inten-sive care unit(SICU) patients conscious-sedation derivative phase .Methods 60 patients after general anaesthesia were divided into routine dose group(dexmedetomidine 1 .00 μg/kg ,group C) ,middle dose group(dexmedetomidine 0 .75 μg/kg ,group M ) and low dose group(dexmedetomidine 0 .50 μg/kg ,group L) ,and the loading time were reset 10 min .sedative effect was evaluated by Ram-say sedation score .Record the mean arterial blood pressure of everyone before administration ,5 min after ,15 min after ,30 min af-ter ,60 min after .Results All patients achieved good conscious-sedation .Compared with pro-administration ,the mean arterial blood pressure of group C descend significantly .The mean arterial blood pressure of group M and L descend significantly ,and then they were recover over time .60 min after the treatment ,the mean arterial blood pressure in group C was significantly lower than group L and goup M (P<0 .05) .Conclusion Small dose dexmedetomidine can achieved good conscious-sedation for SICU patients .It has less influence on hemodynamics .

With our country going into the aging society, burns in the elderly often occur. Studies have shown that the number of elderly burn patients has reached 13% to 20% of the total number of burn patients. As the sensory and cognitive functions are low, skin is thinning, the functions of heart, lung, and kidney are reduced, the immunity is impaired, and other physiological characteristics exist in the elderly, the wounds of elderly burn patients often heal slowly, and the mortality is high. At present, there is still a lack of enough attention to the elderly burn patients. In this review, according to the physiological characteristics of the elderly, for reference to our peers, we make a summary of the treatment of elderly burn patients, such as fluid resuscitation, wound treatment, acute kidney injury management, infection management, and nutritional support.

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.

The various systems and organs of the pediatric body are still in the developmental stage, with immature anatomy and physiology. Pediatric patients with inhalation injury are often in critical conditions, being prone to respiratory difficulties and even evolving into acute respiratory distress syndrome. The changes are rapid with extremely high mortality rate, bringing certain challenges to clinical treatment. This article reviews the causes, characteristics, diagnosis and treatment of pediatric inhalation injury for peer reference.

The fatality rate of patients with critical burns is extremely high, and the clinical treatment is challenging. By reviewing the history on treatment of critically ill burns patients, this article elaborates and analyzes the advanced concepts and technologies at home and abroad about the critical burn treatment in the areas including shock and fluid resuscitation, hypermetabolism and nutrition, inhalation injury and respiratory support, acute kidney injury and continuous renal replacement therapy, wound assessment and management, infection and control, coagulopathy and its prevention and treatment, etc. Furthermore, some thoughts on the future development trend of critical burn treatment are put forward as reference for people in the same field.

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.

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.

Intra-abdominal infection is the second common infectious disease in intensive care unit and inhospital patients, with the mortality rate of 20%-30%. Advances in medicine have not improved the outcomes of patients with intra-abdominal infection, and the increasing multi-drug resistance organism may lead to a deterioration in the prognosis of patients with intra-abdominal infection. Gut microbiota dysbiosis and abdominal cavity infections show an interdependent and mutually aggravating relationship. Intestinal microecological preparations regulate gut flora and are potential therapeutic measures for intra-abdominal infections. The authors review the changes in gut flora during intra-abdominal infection, the effect of gut flora on the prognosis of intra-abdominal infections and the role of intestinal microecological preparations in intra-abdominal infections.

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.