Objective To establish the normative screening model and apply it to screen and manage the stroke risk group ,and to observe its application effect .Methods The screening management team in our department was set up for establishing the norma-tive stroke screening model .Then the stroke screening works were carried out in the outpatient department and the community pop-ulation .The screened groups of stroke high risk were implemented the 1-year control according to the guidelines of stroke screening and intervention .Results 9 631 individuals of stroke risk were screened ,among them 1 786 high-risk patients were screened out with a rate of 18 .55% .The interventions on the risk factors existing in the high-risk patients were implemented .The comparison of blood glucose ,blood pressure ,blood fat ,fat index ,smoking ,physical exercise and reasonable diet before and after interventions in the high-risk patients showed statistically significant differences (P<0 .05) .Conclusion Establishment of the normative manage-ment model of stroke screening is the important guarantee to do a good job of stroke screening and control for high risk group ,and significantly decreases the risk factors for high risk group .

Objective To construct the sequential management model of networked drug-cognitive behavior in patients with chronic insomnia,and to explore the effects of this model on treatment and management of patients with chronic insomnia. Methods A total of 160 patients with chronic insomnia treated from January 2014 to June 2015 were randomly divided into the experimental group and the control group. The experimental group was treated with networked drug-cognitive behavior sequential therapy and management. Through the establishment of patient management files in the network management system,the disease was assessed,treatment programs were developed, remote implementation of 8 weeks of drug-cognitive behavior sequential treatment was conducted,12 months of net-work remote dynamic management and efficacy evaluation was performed. The control group received 8 weeks of traditional medical care with face-to-face drug-cognitive behavior sequential treatment and 12 months outpatient fol-low-up management. Results Comparison of management core indicators:there were significant differences between two groups in number of visiting hospital,exit status,treatment completion and documentation,sleep diary comple-tion,sleep scale completion and patient satisfaction. Comparison of sleep quality:after 2 months of treatment,there was no difference in quality of sleep between two groups; after 12 months of treatment,there were significant dif-ferences in sleep latency,awakening time after sleep,total sleep time and sleep efficiency between two groups. Scale score:after 12 months of treatment,there were significant differences in Pittsburgh sleep quality index,sleep personal beliefs and attitude scale score between two groups. Conclusion Network-based management improves the compliance of patients with chronic insomnia,reduces the loss of follow-up rate,improves sleep cognition,increases sleep quality,saves patients' time and cost,increases patient satisfaction,which is worth promoting in clinical application.

Background and purpose:Although bortezomib has become one of the major therapeutic agents against newly diagnosed or relapsed multiple myeloma (MM), there are some patients who become resistant to bor-tezomib and then relapse, emerging as a major obstacle to long-term survival of MM patients. It has been found that elevation of intracellular cyclic adenosine monophosphate (cAMP) levels could induce cell cycle arrest and apoptosis in MM cells,which has become an interesting approach to MM therapy. This study aimed to investigate possible effects of forskolin combined with bortezomib on bortezomib-resistant myeloma cells and further explore its mechanisms. Methods:The bortezomib-resistant MM cell lines H929-R and primary cells from patients who do not respond to bortezomib were used asin vitro models. The inlfuences of bortezomib and/or forskolin on MM cells were evaluated through cellular morphology, changes of cell distribution and apoptotic rate. Meanwhile, lfow cytometry analysis was used to detect mitochondrial transmembrane potential (ΔΨm) and the expression levels of apoptosis regulators in these cells before and after the treatment were detected by Western blot.Results:Bortezomib (20 nmol/L) synergized with forskolin (50nmol/L) to induce apoptosis of H929-R cells and bortezomib-resistant primary cells. In addition, borte-zomib synergized with forskolin to induce collapse of mitochondrial transmembrane and facilitate the degradation of anti-apoptosis proteins including Bcl-2 and Mcl-1.Conclusion:Bortezomib could synergize with forskolin to induce apoptosis in bortezomib-resistant MM cells.

Objective To study the immunoregulatory effects of thalidomide on the peripheral blood T-lymphocytes of rheumatoid arthritis patients.Methods MTr was used to detect the effects of different thalidomide concentrations on the proliferation of T-cells.Flow eytometry was used to analyze T-cells early apoptosis and the T-cells subsets in different concentration of thalidomide.The mRNA expression of IL-6,IL- 10 and TNF-α was measured by RT-PCR method.Results The level of thalidomide at 500 μg/ml inhibited the proliferation of T-ceils and the CD3+CD28+ expression of T-cell subsets,but promoted the early apoptosis and the CD8+CD152+ expression of T-cell subsets.Thalidomine at any concentration could inhibit the mRNA expression of IL-6,TNF-α.However,the level of thalidomide that could promote the mRNA expression of IL- 10 was 100 μg/ml and 500 μg/ml.Conclusion Thalidomide can inhibit the proliferation of T lymphocytes and the expression of CD3+CD28+ on T-cell subsets.It can promote the early apoptosis and the CD8+CD152+ expression of T-cell subsets.Thalidomide inhibits the mRNA expression of IL-6 and TNF-α but promote the mRNA expression of IL-10.Thalidomide has immuno-regulatory effects on rheumatoid arthritis T-cells.

Objective To explore the value of minute ventilation recovery time (VERT) as a weaning predictor in mechanically ventilated patients with chronic obstructive pulmonary disease (COPD).Methods A prospective study was performed from March 2008 to July 2012.Fifty-two COPD patients under mechanical ventilation for more than 48 hours in our RICU tolerated a spontaneous breathing trial (SBT) and were ready for planned extubation.After SBT,these patients were placed back on their pre-SBT ventilator settings for up to 25 minutes,during which VERT was obtained.VERT was defined as the time for minute ventilation to return to baseline measured before SBT.Respiratory rate,tidal volume,minute ventilation and respiratory rate/tidal volume ratio were also obtained before SBT and just after SBT.Arterial blood gas data were measured and recorded before weaning.According to the weaning outcome,the patients were classified as successful group (40 cases) or failed group (12 cases).VERT and other quantitative variables were compared using t test.A multiple logistic regression was performed to explore possible factors associated with the weaning outcome.The sensitivity and specificity of VERT for predictive capacity in weaning were assessed using ROC cure.Results VERT and respiratory rate after SBT were significantly different between two groups.Multiple logistic regression revealed that VERT was the only predictor associated with weaning outcome (b =0.282,P ＜0.001).The area under ROC curve for VERT was 0.957 (95％ CI:O.907-1.008).With a cut-off value of 10.5 minutes,the sensitivity and specificity of VERT for predicting weaning failure were 1.0 and 0.85,respectively.Conclusions VERT may be a new predictor for extubation and determination of mechanical ventilation weaning in patients with COPD.VERT is a variable to be easily measured thereby being conveniently used in clinical practice.

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Objective To evaluate the role of endothelial nitric oxide synthase (eNOS) in inflammatory responses in mice with ventilator-induced lung injury using gene knockout.Methods Twenty-four male C578L/6J wild type mice and 24 male B6.129P2-Nos3tm1Unc/NJU (eNOS gene knockout) mice,aged 10-12 months,weighing 20-25 g,were randomly assigned into 2 groups (n=12 each) using a random number table:sham operation group (group S) and mechanical ventilation group (group MV).The animals were anesthetized with intraperitoneal 1％ pentobarbital sodium 70 mg/kg,and mechanically ventilated after tracheal intubation.The animals were mechanically ventilated for 4 h (oxygen flow rate 0.5 L/min,FiO2 50％,VT 15 ml/kg,RR 70 bpm,PEEP 2 cmH2O).After 4 h of ventilation,blood samples were obtained from the internal carotid artery for detection of PaO2.The animals were then sacrificed and the lungs were removed for determination of wet/dry lung weight (W/D) ratio,myeloperoxidase (MPO) activity,contents of malondialdehyde (MDA),interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α),and pulmonary microvascular permeability,and for microscopic examination of the pathological changes of lung (with electron microscope).Results Compared with group S of wild type mice,PaO2 was significantly decreased,while W/D ratio,MPO activity,contents of MDA,IL-6,TNF-oα and NO,and pulmonary microvascular permeability were increased in MV groups of wild type and gene knockout mice,and no significant change was found in the parameters mentioned above in group S of gene knockout mice.Compared with group MV of wild type mice,PaO2 was significantly increased,while W/D ratio,MPO activity,contents of MDA,IL-6,TNF-α and NO and pulmonary microvascular permeability were decreased in group MV of gene knockout mice.The pathological changes of lung were significantly attenuated in group MV of gene knockout mice as compared with group MV of wild type mice.Conclusion eNOS is involved in inflammatory responses in mice with ventilator-induced lung injury.

Objective: To investigate protective effects of nicotinamide mononucleotide (NMN) on ethanol-induced DNA damage in L02 cells, so as to provide the evidence for adjuvant therapy of NMN on alcoholic liver diseases. Methods: L02 cells were pretreated with different concentrations of NMN (0, 1, 2, 4 and 8 mmol/L) for 6 h, and then were exposed to 0.4% ethanol for 12 h. The treated cells were divided into the control group, 0.4% ethanol group and different concentrations of NMN groups. Cell viability was analyzed using trypan blue staining for determining the concentration of NMN as a protective agent. The effects of NMN on ethanol-induced DNA damage in L02 cells were evaluated using immunofluorescence detection and reactive oxygen species (ROS) assay. L02 cells were exposed to 0.4% ethanol for 12 h, cultured in a medium containing a protective concentration of NMN, and divided into PBS group and NMN group. Cell viability was detected at 0, 2, 4, 8, 16 and 32 h, and the effects of NMN on repairing ethanol-induced DNA damage were evaluated by alkaline comet assay. Results: The cell viability was lower in 0.4% ethanol group than than in the control group, and was higher in different concentrations of NMN groups than in 0.4% ethanol group (all P<0.05), with no significant difference in the cells viability between 4 mmol/L and higher concentrations of NMN groups and the control group (all P>0.05). Therefore, 4 mmol/L NMN was selected as a protective agent. The cell tail moments, relative immunofluorescence intensities of γH2AX and relative levels of ROS were higher in 0.4% ethanol group than in the control group, and lower in 4 mmol/L and higher concentrations of NMN groups than in 0.4% ethanol group (all P<0.05). The cell viability was increased and the cell tail moment was shortened with the increase of 4 mmol/L NMN intervention time; and the cell viability in 4 h and more of NMN groups were higher, and the cell tail moment were lower than that in PBS group (all P<0.05). Conclusions NMN attenuates DNA damage in a dose-dependent manner and promotes the repair of DNA damage in a time-dependent manner. NMN has a protective effect on ethanol-induced DNA damage in hepatocytes.

Objective To determine the viral etiology and its epidemic features of community-acquired pneumonia ( CAP) among pediatric inpatients in Guangzhou.Methods A total of 1 539 children with CAP admitted in Guangzhou Women and Children’ s Medical Center during June 2012 and June 2013 were enrolled in the study.Throat swab specimens were collected, and fluorescence quantitative polymerase chain reaction ( FQ-PCR) was performed to detect 11 respiratory pathogens.SPSS 17.0 was used for data processing, and χ2 test was performed to compare the infection rates among different groups.Results Among 1 539 patients, 550 cases (35.7%) were infected with at least one pathogen, and 101 (6.6%) were infected with two or more pathogens.The most popular viral etiologies were respiratory syncytial virus (RSV) (102, 6.6%), rhinovirus (RHV)(101, 6.6%), adenovirus (ADV) (78, 5.1%), influenza virus A (IVA) (78, 5.1%) and bocavirus (HBOV) (74, 4.8%).RSV infection often occurred in children with age≤3 years, while ADV or IVA infection often occurred in those with age >3 years.RSV infection rate peaked in winter and spring, IVA infection rate peaked in spring and summer, while ADV and HBOV infection rates peaked in summer.The rate of multiple infections in critically ill children (22/135, 16.3%) was significantly higher than that in other CAP patients (79/1 404,5.6%,χ2 =116.049, P<0.01).Conclusions Viral infection is common in pediatric inpatients with CAP, and RSV infection is the most popular.Multiple infections are more often to cause critical conditions.