Objective To explore the implementation styles on the therapeutic effects on the neurosurgical intensive care unit (NICU) patients. Methods Patients were enrolled during February 3, 2015 to February 3, 2016. The key point time was August 3, 2015 when the treatment in our NICU was fully implemented by NICU professional doctors. Based on this time point, all the enrolled patients were divided into non-NICU professional doctor implementing (NNPDI) group and NICU professional doctor implementing (NPDI) group. Thus non-NICU professional doctors and professional doctors were the leaders of diagnosis and treatment in tow groups. The length of hospital stay, complications, prognosis and other therapeutic outcomes were compared between two groups. Results The length of hospital stay was longer in NPDI group than that in NNPDI group (P<0.05). The incidence of water-electrolyte imbalance was lower in NPDI group than that in NNPDI group (P<0.05). There were no significant differences in the incidence of the ventilator-associated pneumonia (VAP), the hepatic and renal insufficiency, the intracranial infections and stress ulcers between the two groups (P>0.05). The proportion of referral to other wards and fatality rate were both lower in NPDI group than those in NNPDI group (P<0.05). And the discharge rate from NICU was higher in NPDI group than that of NNPDI group (P<0.05). There was no significant difference in the rate of patients left hospital without treatment between the two groups (P>0.05). Conclusion The NICU professional doctor implementing may be contribute to, at least in part, the improving of prognosis of NICU patients without obvious advantages in most complications. The level of professional management remains to be improved.

Objective To study the effect of small interfering ribonucleic acid (siRNA) silencing apoptosis signal-regulating kinase 1 (ASK1) on inflammatory response of lipopolysaccharide-induced alveolar epithelial A549 cells and its mechanism.Method Cell inflammation model of A549 cells was induced by lipopolysaccharide.The expression of ASK 1 in A549 cells was silenced by liposome transfection of siRNA.The mRNA and expression levels of ASK1,interleukin 6 (IL-6),interleukin 8 (IL-8) and tumor necrosis factor alpha (TNF-α) in A549 cells were detected by immunoblotting,real-time fluorescence quantitative polymerase chain reaction and enzyme-linked immunosorbent assay.Result The expression of IL-6,IL-8 and TNF-α in the experimental group was significantly higher than that in the control group (P＜0.001),which indicated that the inflammatory model of A549 cells was successfully constructed.The mRNA level and expression of ASK1 in the interference group was significantly lower than that in the negative control group and the blank control group (P＜0.01),indicating that silencing ASK1 was also successful.The expressions of IL-6,IL-8 and TNF-α in the interference group (0.37±0.04,0.32±0.04,0.48 ±0.13) were significantly lower than those in the negative control group (1.04±0.11,1.22±0.19,0.93±0.14) and the blank control group (1.01±0.14,1.01 ±0.23,1.02±0.25).The expression of IL-6,IL-8 and TNF-α protein in the interference group (pg/ml) (122.6± 11.0,537.2±42.4,159.2± 19.6) were also significantly lower than those in the negative control group (267.4±20.4,1 289.8±55.3,327.0±26.3) and blank control group (246.6±18.7,1 300.3±35.6,325.2± 18.3),with significant difference (P＜0.05).There was no significant difference in each value between negative control group and blank control group (P＞0.05).Conclusion Silencing ASK1 by siRNA can down-regulate the expression of IL-6,IL-8 and TNF-α in A549 cells,suggesting that ASK 1 may be involved in the regulation of lipopolysaccharide-induced inflammation in A549 cells.

Objective To investigate the role of signal transducer and activator of transcription 3 (STAT3) on the expression of surfactant proteins (SP) in alveolar epithelial cells line A549.Methods STAT3 overexpression lentivirus vector was constructed and transfected into A549 cells.Three small interfering RNAs (siRNA) were chemically synthesized and transfected into A549 cells by Lipofectamine 3000 to construct cells that silenced STAT3.The expression of STAT3,SP-A,SP-B,SP-C and SP-D were detected by Real-time PCR and Western blot.Results In A549 cells,over-or under-regulation of STAT3 were constructed successfully.When STAT3 was rendered over-expressed,the expression of SP-A,SP-B,SP-C,SP-D mRNA was significantly increased compared with Mock group(P ＜ 0.05).The proteins were found to be significantly increased as well.By contrast,when STAT3 was under-expressed,SP was down-regulated (P ＜ 0.05).Conclusion STAT3 regulates the expression of pulmonary surfactant proteins in A549 cells.Over-expression of the STAT3 gene promotes the expression of SP,and its under-expression inhibited it.