Objective To analyze acinetobacter Baumanii infections in ICU and explore the nursing strategies.Method The clinical data of 5310 ICU patients infected with acinetobacter Baumanii in our hospital were retrospectively analyzed.Results Among the 5310 patients in the ICU,26 were infected by acinetobacter baumanii with an incidence of 0.5%,with 46.2%patients contracted cerebral hemorrhage,38.5%intracerebral tumor,92.3%infection by multi-drug resistant bacteria and.All patients were managed with artificial ventilation and 84.6%patients were hospitalized in ICU for over 7 days.Conclusions The nursing strategies includes reasonable use of antibiotics,active treatment of primary diseases,rigid control of disinfection and isolation,attaching importance to hand hygiene and strict implementation of nursing practice,which are important for preventing and controling the infection of acinetobacter baumanii.

Objective: To observe the changes of heart-type fatty acid binding-protein(H-FABP) in the femoral vein(periphe ral blood) and urine of rats with myocardial infarction in different postmortem intervals. Methods: Acute myocardial infarction (AMI) was duplicated by ligating the anterior branch of the left coronary artery following the method of Johns in rats. Concentrations of H-FABP were detected with enzyme-linked immuno-sorbent assay (ELISA). Results: The concentrations of H-FABP in experiment group were obviously higher than that in control group. Along with the time, the concentrations of H-FABP in experiment group rose consistently, the concentration of H-FABP in 12 h group rose markedly, and it was obviously higher than in 48h that in 24h. The H-FABP concentrations in urine of the experiment group were obviouslyhigher than the one in control group. The urine concentrations of H-FABP in experiment group increased by wavy in postmortem intervals, the concentration of H-FABP in (6h) group was obviouslyhigher than that in 0h group, 12h and 24h postmortem, the H-FABP concentrations decreased, but still higher than that of 0h group and 48h group, the concentration of H-FABP rose markedly and washigher than 6h group. Conclusion: Affected by autolysis, the H-FABP concentrations of plasma and urine appeared abnormal raise and can not be used in postmortem diagnosis of AMI.

Objective To evaluate the effects of mechanical stretch preconditioning on pathological stretch-induced activation of nuclear factor kappa B (NF-κB) and signal transducer and activator of transcription 3 (STAT3) signaling pathways in human type Ⅱ alveolar epithelial cells.Methods Human type Ⅱ alveolar epithelial cell line A549 cells cultured in vitro were randomly divided into 3 groups (n =24 each) using a random number table: control group (group Ⅰ), pathological stretch group (group Ⅱ), and mechanical stretch preconditioning group (group Ⅲ).In group Ⅰ , A549 cells were cultured routinely without receiving pathological stretch.In group Ⅱ , A549 cells were exposed to 20％ cyclic stretch at 0.3 Hz for 6 h.In group Ⅲ , A549 cells were exposed to 5％ cyclic stretch at 0.3 Hz for 60 min, and then exposed to 20％ cyclic stretch at 0.3 Hz for 6 h.After the end of the treatment, the cells were collected for determination of the cell viability (by methyl thiazolyl tetrazolium assay) and lactate dehydrogeuase (LDH)release (by colorimetric method).The concentrations of tumor necrosis factor-alpha (TNF-α),interleukin-8 (IL-8) and high mobility group box 1 (HMGB1) in the culture medium were detected using enzyme linked immunosorbent assay.The expression of total NF-κB, phosphorylated NF-κB, total STAT3 and phosphorylated STAT3 was detected using Western blot.The ratios of phosphorylated NF-κB to total NF-κB and phosphorylated STAT3 to total STAT3 were calculated to reflect the activation.Results Compared with group Ⅰ , the cell viability was significantly decreased, the amount of LDH released was increased, and the concentrations of TNF-α, IL-8 and HMGB1, and activation of NF-κB and STAT3 were increased in Ⅱ and Ⅲ groups.Compared with group Ⅱ , the cell viability was significantly increased, the amount of LDH released was decreased, and the concentrations of TNF-α, IL-8 and HMGB1, and activation of NF-κB and STAT3 were decreased in group Ⅲ.Conclusion The mechanism by which mechanical stretch preconditioning attenuates pathological stretch-induced damage to human type Ⅱ alveolar epithelial cells is related to inhibited activation of NF-κB and STAT3 signaling pathways.

Objective To evaluate the role of spinal RhoA/ROCK signaling pathway in the development of lipopolysaccharide (IP)-induced inflammatory pain(IP) in rats.Methods Fifty-two male Sprague-Dawley rats, weighing 180-220 g, were equally randomized into 4 groups using a random number table: normal saline group (group NS) , LPS group, RhoA inhibitor C3 exoenzyme group (group LC) , and ROCK inhibitor Y27632 group (group LY).Inflammatory pain was induced by injecting LPS 25 μl (300 ng) into the plantar surface of hindpaws in IP, LC and LY groups, while the equal volume of normal saline was injected instead in NS group.C3 exoenzyme 10 pg and Y27632 10 nmol were injected intrathecally at 30 min prior to LPS administration in LC and LY groups, respectively.Before LPS injection (T0) , and at 1, 3, 5, 12 and 24 h after LPS injection (T1-5) , the mechanical and thermal pain thresholds were measured.Five rats in each group were sacrificed after pain thresholds were measured at T3, and L4.5 segments of the spinal cord were removed for determination of tumor necrosis factor-alpha (TNF-α) and interleukin-1 beta (IL-1β) mRNA expression in spinal dorsal horns by real-time reverse transcriptase-polymerase chain reaction.Results Compared with group NS, the mechanical and thermal pain thresholds were significantly decreased at T2-5in IP, LC and LY groups, and TNF-α and IL-1β mRNA expression was up-regulated at T3 in IP group.Compared with group IP, the mechanical and thermal pain thresholds were significantly increased at T2-5, and TNF-α and IL-1β mRNA expression was down-regulated at T3 in LC and LY groups.Conclusion Spinal RhoA/ROCK signaling pathway is involved in the development of LPS-induced IP in rats.

A gram-negative bacillus was isolated from the bodies of dead clams among clambanks along the south beach of Jiangsu province. It was confirmed to the Vibrio furnissii by morphological and biochemical characteristic examinations. This isolate grows well in clam's body fluid media and may multiply rapidly in sea-water at temperature about 25—37℃. It is of high toxicity. The healthy clams were all diseased with the same syndrome and died as natural illness by inoculate them with the isolate. It is considered that the large enormous death of clams along the south beach of Jiansu province is concerned with the wide spreading of the clam's infectious disease caused by Vibrio furnissii which hasn't been reported both internal and abroad.

Objective This study aims to evaluate the effect of joint training on professional core competencies of Intensive Care Unit (ICU) nurses.Methods Nurses enrolled in Joint Training Program (the experimental group) between 2007 to 2009 were interviewed with questionnaire and compared with those received general training (the control group).Data were collected before and after 10 months of training.Scores of ICU nurse core competencies from the two groups were analyzed and compared.Restults Comparing with the control group,scores of the experimental group showed statistical differences on total score,theory dimension,technical dimension and 54 items.Conclusions Joint training could improve the professional core competencies of ICU nurses,especially the competences of management and application of nursing to critically ill patients and ICU special skills.

Objective To evaluate the accuracy of respiratory variations of internal jugular vein (IJV) in monitoring fluid responsiveness in patients undergoing radical gastrectomy for gastric cancer.Methods Fifty American Society of Anesthesiologists physical status Ⅰ or Ⅱ patients of both sexes,aged 40-64 yr,scheduled for elective radical gastrectomy for gastric cancer,were enrolled in this study.Before induction of anesthesia,the hemodynamic parameters such as heart rate,central venous pressure,cardiac index,stroke volume index (SVI),stroke volume variation and respiratory variation of IJV were recorded after haemodynamics was stable and were recorded again at 10 min after endotracheal intubation,and a loading dose of 6％ 130/0.4 hydroxyethyl starch 7 ml/kg was infused over 15 min.The parameters mentioned above were recorded within 5 min after loading dose.Patients were divided into 2 groups according to the percentage of increase in SVI (△SVI) after volume expansion:△SVI≥ 15％ was considered to be a positive response (responder group) and △SVI＜15％ was considered to be a negative response after volume expansion (non-responder group).Results The area under the receiver operating characteristic curve of respiratory variations of IJV in monitoring fluid responsiveness and 95％ confidence interval were 0.852 (0.744-0.961).Respiratory variation of IJV 24.6％ was considered as the cut-off value and used to monitor fluid responsiveness,and the sensitivity and specificity were 67.6％ and 92.3％,respectively.Conclusion Respiratory variation of IJV can be considered as an effective index in monitoring fluid responsiveness in the patients undergoing radical gastrectomy for gastric cancer.

BACKGROUNDTo sequence, analyze and express the nucleotide sequences of S and M segments of hantavirus strain 84Fli.

METHODSS and M segments of hantavirus 84Fli strain were amplified by RT-PCR, the PCR products were cloned into plasmid pCR2.1-TOPOr. Three clones of each segment which have been sequenced were randomly selected. The coding region of S and M segments were amplified by PCR, and cloned into expressing vector pcDNA3.0. Transient expression of nucleocapsid protein, G1 and G2 glycoproteins in COS7 cells were performed by Lipofectin transfection. The expression of NP, G1 and G2 have been conformed by using immunofluorescence, Western blot and immuno-precipitation methods.

RESULTSThe full length S and M segments cDNA have been amplified and cloned. The S and M segments of hantavirus strain 84Fli contained 1 688 and 3 616 nucleotides respectively.

CONCLUSIONSDeduced amino acid sequences of NP and glycoproteins revealed high homologue to other Hantaan viruses. NP, G1 and G2 proteins of 84Fli can be transiently expressed in COS7 cells.

Animals ; COS Cells ; metabolism ; Cloning, Molecular ; Gene Expression ; Glycoproteins ; biosynthesis ; Hantavirus ; genetics ; metabolism ; Nucleocapsid Proteins ; biosynthesis ; Sequence Analysis ; Viral Proteins ; biosynthesis

Objective To investigate the expressions of a disintegrin and metalloprotease 17 (ADAM17) and epidermal growth factor recepter (EGFR) in human esophageal squamous cell carcinoma (ESC),and to explore their relationship with clinicopathological characteristics.Methods The paraffin specimens in postoperative pathological tissues of 66 ESC patients in the Third People's Hospital of Hefei from January 2013 to December 2017 were selected.Expressions of ADAM17 and EGFR proteins were examined by using immunohistochemistry in 66 cases of ESC tissues and 33 cases of adjacent tissues of the tumors.The relationship of ADAM17 and EGFR with clinicopathological features was analyzed.Kendall method was used to detect the expression correlation of ADAM17 and EGFR.Results The positive rate of ADAM17 protein in ESC tissues was higher than that in the adjacent tissues of the tumors [68.2 ％ (45/66) vs.33.3 ％ (11/33),x2 =10.874,P =0.001].The positive rate of EGFR protein in ESC tissues was higher than that in the adjacent tissues of the tumors [66.7 ％ (44/66) vs.39.4 ％ (13/33),x2 =6.699,P =0.01].The expressions of ADAM17 and EGFR protein were related with ESC pathological TNM staging,infiltration depth,lymph node metastasis (x2 =4.797,4.890,6.089;8.790,8.766,10.154,respectively,all P ＜ 0.05).ADAM17 expression was positively correlated with EGFR protein (r,=0.368,P ＜ 0.05).Conclusions ADAM17 and EGFR are highly expressed in human ESC.Besides,ADAM17 and EGFR have the interaction in the occurrence and development of esophageal cancer.Joint detection may help to determine the degree of metastasis and evaluate prognosis.

Objective To evaluate the relationship between the shedding of syndecan-4(SDC-4) in lung tissues and ventilator-induced lung injury in rats. Methods Thirty pathogen-free healthy adult male Wistar rats, weighing 220-250 g, were divided into 3 groups(n=10 each)using a random number table:control group(group C), mechanical ventilation with traditional tidal volume(VT)group(group T-VT) and mechanical ventilation with high VTgroup(group H-VT). The animals were anesthetized with pento-barbital sodium and tracheostomized. The rats kept spontaneous breathing in group C. The rats were me-chanically ventilated for 4 h with the VTset at 6 ml∕kg in group T-VT and with the VTset at 40 ml∕kg in group H-VT. Blood samples were collected immediately after the end of ventilation for measurement of serum SDC-4 concentrations by enzyme-linked immunosorbent assay. The left lung was lavaged, and broncho-alveolar lavage fluid was collected for determination of interleukin-1beta(IL-1β), IL-18, tumor necrosis factor-alpha and SDC-4 concentrations by enzyme-linked immunosorbent assay. The lungs were removed for determination of the wet to dry weight ratio and expression of SDC-4 protein and mRNA in lung tissues(by Western blot and real-time polymerase chain reaction, respectively)and for examination of the pathological changes. The lung injury scores were recorded. Results Compared with group C, the wet to dry weight ratio, lung injury scores, concentrations of IL-1β, IL-18, tumor necrosis factor-alpha and SDC-4 in bron-cho-alveolar lavage fluid and concentrations of SDC-4 in serum were significantly increased, the expression of SDC-4 mRNA was up-regulated, and the expression of SDC-4 was down-regulated in group H-VT(P<005), and no significant change was found in the parameters mentioned above in group T-VT(P>005).Marked pathological changes of lung tissues were found in group H-VT. Conclusion A large shedding of SDC-4 in lung tissues may be involved in the pathophysiological mechanism of ventilatior-induced lung injury in rats.