Objective:To investigate the application of pulse contour cardiac output (PiCCO) monitoring technology in fluid resuscitation of severe burn patients in shock period.Methods:From January 2015 to December 2019, 33 patients with severe burns who were hospitalized in Guangzhou Red Cross Hospital, meeting the inclusion criteria, were recruited into a retrospective cohort study with their clinical information collected. The patients were divided into PiCCO monitoring group with 15 cases (13 males and 2 females, aged (43±13) years) and routine monitoring group with 18 cases (14 males and 4 females, aged (39±9) years) according to the monitoring method used. After admission, all the patients were rehydrated following the rehydration formula of the Third Military Medical University for shock period. In routine monitoring group, the fluid resuscitation of patients was performed by monitoring indicators such as urine volume and blood pressure, while PiCCO monitoring was performed among patients in PiCCO monitoring group, and their fluid resuscitation was guided by the patient′s condition and the hemodynamic parameters (without pursuing normal levels of the parameters) of PiCCO monitoring on the basis of normal monitoring indicators in routine monitoring group. The colloids coefficients, the electrolyte coefficients (compared with the corresponding rehydration formula value of 0.75 mL·kg -1·% total body surface area (TBSA) -1 of the Third Military Medical University for shock period during the first 24 h post injury), the total rehydration coefficients, and the urine volumes during the first and second 24 h post injury, the lactic acid level, the base excess level, and the oxygenation index at admission and 24, 48 h after admission, and the mechanical ventilation time, the wound healing time, and the death ratio of patients in the two groups were recorded. The cardiac index, the global end-diastolic volume index (GEDVI), the intrathoracic blood volume index (ITBVI), the extravascular lung water index (EVLWI), and the systemic vascular resistance index (SVRI) of patients in PiCCO monitoring group at post injury hour 24, 48, and 72 and the abnormal cases were recorded. Data were statistically analyzed with Fisher′s exact probability test, independent-sample or one-sample t test, analysis of variance for repeated measurement, and Bonferroni correction. Results:During the first 24 h post injury, the colloids coefficients of patients in PiCCO monitoring group was (0.69±0.15) mL·kg -1·%TBSA -1, which was significantly less than (0.85±0.16) mL·kg -1·%TBSA -1 in routine monitoring group ( t=-2.612, P<0.05). Compared with the rehydration formula value of the Third Military Medical University for shock period, only the colloids coefficient of patients in routine monitoring group during the first 24 h post injury was significantly increased ( t=2.847, P<0.05). There were no statistically significant differences between the two groups in the colloids coefficients of patients during the second 24 h post injury, or the electrolyte coefficients, the total rehydration coefficients, the urine volumes of patients during the first and the second 24 h post injury ( t=0.579, -0.011, 0.417, -1.321, -0.137, 0.031, 1.348, P>0.05). The lactic acid level, the base excess level, the oxygenation index of patients at admission and 48 h after admission, and the oxygenation index of patients at 24 h after admission between the two groups were similar ( t=-1.837, 0.620, 0.292, -1.792, 1.912, -0.167, 1.695, P>0.05). The levels of lactic acid and base excess of patients in PiCCO monitoring group were (4.8±1.4) and (1.2±5.5)mmol/L, respectively, which were significantly better than (7.0±1.5) and (-2.8±3.0) mmol/L in routine monitoring group at 24 h after admission ( t=-3.904, 2.562, P<0.05 or P<0.01). There were no statistically significant differences between the two groups in the mechanical ventilation time or the wound healing time of patients ( t=-0.699, -0.697, P>0.05), or the death ratio of patients ( P>0.05). In PiCCO monitoring group, the GEDVI, and the ITBVI of patients were lower than the normal low values at post injury hour 24 and 48, which were in the normal range at post injury hour 72; the cardiac index of patients increased gradually and recovered to normal at post injury hour 48; the SVRI of patients increased significantly at post injury hour 24 and then gradually decreased to normal; the EVLWI average of patients at all time points post injury were less than 10 mL/kg. At post injury hour 24, most of the hemodynamic parameters of more than or equal to 8/15 patients in PiCCO monitoring group were abnormal, and the abnormal proportion decreased later. Conclusions:On the basis of traditional monitoring indicators, the use of PiCCO monitoring technology combined with the patient′s condition (without pursuing normal levels of the parameters) in guiding the fluid resuscitation in severe burn patients can reduce the usage of colloid and better improve tissue perfusion, with the resuscitation effect being better than conventional monitoring.

Objective To explore the pressure sources of new head nurses , so as to provide them the adapting interventions .Methods Face-to-face and semi-structured interviews of phenomenological method were carried out to collect data .Then, 7-step Colaizzi method and the theory of two-dimensional structure of pressure were used to analyze the data .Results The main challenge stressors of new head nurses were safety control of nursing, management ability, time management, interpersonal relationship and self-improvement.The main hindrance stressors were role maladjustment and lack of pre-job training.Conclusions Executives of head nurses should conduct pre-job training and give some guidance for new head nurses , so as to stimulate the promotion function of challenge stressors and eliminate the obstructive role of the hindrance stressors , in order to help them to adapt to the job as soon as possible .

Purpose To investigate the effect of MYD88 gene overexpression on the proliferation and apoptosis of human diffuse large B cell lymphoma(DLBCL)cells,and to prelimi-narily explore the mechanism of MYD88 gene action.Methods PEGFP-C2-MYD88 overexpressing MYD88 L265P gene was transfected into DLBCL cells by plasmid transfection.The exper-iment was divided into blank control group,negative control group and MYD88 L265P overexpression group.The fluores-cence expression of MYD88 L265P after overexpression was ob-served under inverted fluorescence microscope.RT-PCR and Western blot were used to detect the mRNA and protein expres-sion of MYD88 L265P,IRAK4,NF-κB and BCL2 in DLBCL cells before and after overexpression of MYD88 L265.CCK8 method was used to detect DLBCL cells proliferation and Ho-echst staining was used to detect DLBCL cells apoptosis.Re-sults After overexpression of MYD88 L265P,compared with the blank control group(0.670 4±0.017 5)and the negative control group(0.715 3±0.019 6),the MYD88L265P overex-pression group(1.157 2±0.010 2)increased significantly,with statistical significance(all P＜0.05).After overexpression of MYD88 L265P,compared with the blank control group(0.69 ±0.04)and the negative control group(0.81±0.07),the MYD88L265P overexpression group(0.48±0.05)was signifi-cantly decreased,with statistical significance(all P＜0.05).After overexpression of MYD88 L265P,compared with the blank control group(mRNA:1.0158±0.0115,0.987 3±0.010 2,1.007 6±0.015 3,protein:0.183 4±0.058 9,0.096 8± 0.015 7,0.147 5±0.0418)and negative control group(mR-NA:0.9132±0.0098,1.0032±0.0156,0.9327± 0.011 2,protein:0.187 9±0.042 3,0.088 9±0.0513,0.134 8±0.050 1),the mRNA(3.243 2±0.013 6,2.976 6 ±0.0213,1.585 9±0.019 8)and protein expressions(0.452 7±0.052 4,0.218 9±0.047 5,0.301 4±0.059 8)of IRAK4,NF-κB and anti-apoptosis protein BCL2 in MYD88L265P overexpression group were significantly increased,which was statistically significant(all P＜0.05).Conclusion After overexpression of MYD88 L265P,the apoptosis rate of DLBCL cells decreased and the cell proliferation rate increased.The mechanism may be related to the mutation of MYD88 L265P gene,activation and amplification of NF-κB pathway,and pro-motion of the overexpression of antiapoptotic protein BCL2.