Objective To investigate the activities associated with nurses’occupational exposure to bloodborne pathogens and the source patients’infection status during blood collection process,so as to provide a basis for developing occupational exposure prevention strategies.Methods Data about occupational exposure to bloodborne pathogens during blood collection process in a hospital from August 2011 to September 2013 were monitored.Results A total of 89 times of bloodborne ex-posure occurred among HCWs,including 75 times of arterial blood collection and 14 venous blood collection.The top three procedures of occupational exposures were rebounding of needles after needles were pulled out (28.09%,n=25),concen-trated cleaning up of rubbish at the end of blood collection (20.22%,n=18),and touching blood and body fluids by skin and mucous membrane (14.61%,n=13).48.31% (n=43)source patients infected with at least hepatitis B virus,hepati-tis C virus ,hepatitis E virus,Treponema pallidum,and human immunodeficiency virus ,51.69%(n=46)source patients were not infected ,after proper handling,none of nurses were infected during blood collection .Conclusion Developing safe blood-withdraw needle,putting sharp instrument into sharp instrument container,wearing gloves,and intensifying training of standard and occupational precaution are important strategies for the reducing of the occurrence of bloodborne exposure of clinical nurses during blood collection process .

Objective To research the mechanism of High Volume Hemofiltration (HVHF) on acute lung injury (ALI) induced by LPS in dogs. Methods After injection of LPS (650 ?g/kg) via central vein within 30 min, Sixteen healthy hybrid male dogs were divided into control group and treatment group randomly (n=8). PaO2、PaCO2 in artery blood were recorded. Contents of TNF-?、IL-6 and IL-10 in plasm were measured by radioimmunity. The activity of NF-?B in lung homogenate was measured by flow cytometer. The content of surfactant protein B (SP-B) in lung homogenate was measured by Western-blotting.Changes of lung histopathology was observed via electron microscopy. Results After injection of LPS, PaO2 and PaO2/FiO2 began to decrease. PaO2 and PaO2/FiO2 in treatment group kept higher than that in control group (P

Objective To evaluate the efficacy of early continuous high-volume-hemofiltration in the treatment of patients with severe acute pancreatitis (SAP).Methods Based on the method of prospective,randomized and controlled clinical trial,60 patients with SAP between January 2005 and July 2011 from the First Affiliated Hospital of Nanchang University were divided into control group and hemofiltration group.The hemofiltration group was treated with early continuous high-volume-hemofiltration and not in the control group.The changes of vital signs,clinical symptoms and laboratory indicators were compared between the two groups before and after the treatment.Results After hemofiltration,the clinical symptoms such as abdominal pain,fever,tachycardia and respiratory distress in hemofiltration group were significantly remitted compared to those in the control group (P ＜0.05).The APACHE Ⅱ score (13.3 ± 1.0 vs 14.1 ± 1.2) and the level of TBil[(20.4±11.3) μmol/L vs (28.1 ±10.9) μmol/L],creatinine[(178.7 ±71.8)μmol/L vs (215.6 ± 51.3) μmol/L],blood urea nitrogen[(10.1 ± 5.6) mmol/L vs (13.2 ± 3.8) mmol/L] and ALT[(51.3 ± 13.2) U/L vs (62.5 ±14.3) U/L] were decreased compared to those in the control group (all P values ＜0.05).The level of PaO2/FiO2(197.3 ±32.4 vs 178.3 ±31.7) was increased (P ＜ 0.05).After hemofiltration,heart rate was decreased gradually (P ＜ 0.05) in the hemofiltration group than in the control group.Mean artery pressure (mAP) increased gradually (P ＜ 0.05) in the hemofiltration group than in the control group.Conclusion Early continuous high-volume-hemofiltration has significant effects on the treatment of SAP including the improvement of clinic symptoms,the blockade of development from systemic inflammatory response syndrome (SIRS) to multiple organ dysfuction syndrome(MODS),improvement of organ function and prevention from the complications.It may become one of the important therapies for SAP.

ObjectiveTo investigate the protective effect of transfected microRNA-146a (miR-146a) on mice with sepsis-induced acute lung injury (ALI) in vivo.Methods Twenty-four healthy male BALB/C mice were randomly divided into sham group, sepsis group, transfection group and transfection control group, eachn = 6. Mice in transfection group were given miR-146a agomir loaded by in vivo-jetPEITM via airway before reproduction of model, and mice in transfection control group were given negative control loaded by in vivo-jetPEITM only via airway. The septic model was reproduced by cecal ligation and puncture (CLP) 12 hours after transfection , and the mice in the sham group underwent laparotomy and closure only without ligation and puncture of the cecum. The mice of each group were sacrificed at 24 hours post-operation. The expression of miR-146a in lung tissue was determined by real time fluorescence quantitative reverse transcription-polymerase chain reaction (RT-qPCR), and the quantity of tumor necrosis factor-α (TNF-α) in the bronchial alveolar lavage fluid (BALF) was determined with enzyme-linked immunosorbent assay (ELISA). The wet/dry ratio of lung (W/D) was determined. The pathohistological changes in the lung were observed and scored. Results The expression of miR-146a showed a significant increase in sepsis group, transfection group and transfection control group, which were (3.56±0.43), (27.64±3.46) and (3.72±0.54) folds of that in sham group, respectively (P< 0.05 orP< 0.01). The miR-146a expression in transfection group was significantly increased compared with sepsis group and transfection control group (bothP< 0.01), but no statistical difference in the expression was found between sepsis group and transfection control group (P> 0.05). Compared with the sham group, higher level of TNF-αin the BALF was found in the sepsis group, transfection group and transfection control group (ng/L: 511.65±43.47, 305.74±34.76, 492.27±42.21 vs. 50.72±7.23, allP< 0.01). The level of TNF-α in transfection group was significantly lower than that in sepsis group and transfection control group (bothP< 0.01). Compared with the sham group, the W/D ratio of lung in sepsis group, transfection group and transfection control group showed a significant increase (6.11±0.32, 5.02±0.29, 6.05±0.43 vs. 4.18±0.10, allP< 0.01). The W/D ratio of lung in transfection group was significantly lower than that of sepsis group and transfection control group (bothP< 0.01). The lung injury score of transfection group was significantly lower than that of sepsis group and transfection control group (6.12±0.75 vs. 10.53±1.52, 9.73±1.08, bothP< 0.01).Conclusions miR-146a agomir loaded by in vivo-jetPEITM instillation into airway was able to increase the expression of miR-146a in the lung tissue of septic mice. Up-regulation of miR-146a inhibit the release of the inflammatory cytokine TNF-α stimulated by sepsis, and alleviate inflammatory reaction and lung tissue injury in mice with sepsis-induced ALI.

ObjectiveTo observe the effect of acetylcholine (ACh) on lipopolysaccharide (LPS) induced inflammatory model of rat alveolar macrophages, and to observe the effect of the acetylcholinesterase inhibitor physostigmine (Phy) on the anti-inflammatory effect of ACh.Methods The rat alveolar macrophages NR8383 were cultured in vitro, which were divided into five groups: blank control group, LPS group (stimulated with 1 mg/L LPS for 12 hours), LPS+ ACh group (0.01, 0.1, 1, 10, 100μmol/L of ACh were added for 5 minutes before LPS stimulation), LPS+ Phy group (1 mmol/L Phy was added for 5 minutes before LPS stimulation), and LPS+ ACh+ Phy group (1 mmol/L Phy and 10μmol/L ACh were added for 5 minutes before LPS stimulation). The supernatants were collected in each group, the enzyme-linked immunosorbent assay (ELISA) was used to assay the contents of tumor necrosis factor-α (TNF-α), interleukins (IL-1β, and IL-6). The activity of acetylcholine esterase (AChE ) in the supernatant was also determined.Results① The contents of TNF-α (ng/L: 605.09±57.13 vs. 34.07±8.62), IL-1β (ng/L: 377.09±28.55 vs. 32.33±10.62) and IL-6 (ng/L: 558.04±77.45 vs. 42.62±11.21) in the LPS group were significantly higher than those in the blank control group (allP< 0.05). These results indicated that the inflammatory model of rat alveolar macrophages was constructed successfully.② ACh with the final concentrations of 0.01, 0.1, and 1μmol/L had less influence on the production of TNF-α, IL-1β and IL-6 in the culture supernatants of alveolar macrophages stimulated with LPS compared with LPS group (allP> 0.05). Nevertheless, 10μmol/L and 100μmol/L ACh notably reduced the production of TNF-α (ng/L: 451.19±30.67, 332.19±32.19 vs. 604.96±22.56), IL-1β(ng/L: 261.08±24.78, 143.98±28.39 vs. 367.06±10.44) and IL-6 (ng/L: 342.75±54.60, 235.48±29.75 vs. 562.69±63.34) in the culture supernatants compared with the LPS group (allP< 0.05).③ The activity of AChE in the LPS group was significantly higher than that in the blank control group (kU/L: 5.21±0.63 vs. 3.09±0.10,P< 0.05). The activity of AChE was successfully inhibited by 1 mmol/L acetylcholinesterase inhibitor Phy pretreatment compared with that in the LPS group (1.51±0.12 vs. 5.21±0.63,P< 0.05).④ The level of TNF-α (ng/L: 183.17±35.44 vs. 451.19±30.67), IL-1β (ng/L: 91.49±12.27 vs. 261.08±24.78) and IL-6 (ng/L: 108.17±22.82 vs. 342.75±54.60) in the culture supernatants of LPS+ ACh+ Phy group was significantly decreased as compared with LPS+ ACh group (allP< 0.05).Conclusions ACh with the final concentrations of 10μmol/L and 100μmol/L can inhibit the LPS induced inflammatory reaction in alveolar macrophages. The acetylcholinesterase inhibitor Phy can reinforce the ACh-mediated anti-inflammatory effect on alveolar macrophages inflammatory model.

BACKGROUND:Macrophage migration inhibitory factor (MIF) is a multi-potent cytokine that makes considerable contribution to the regulation of inflammatory response and immune response in the body. MIF rs1007888 is associated with various inflammatory diseases, but the correlation between rs1007888 and coronary heart disease in the Kazakhs of China has been rarely explored. OBJECTIVE:To investigate the relationship between rs1007888 gene polymorphisms in MIF gene and coronary heart disease in the Kazakhs from Xinjiang Uygur Autonomous Region, China. METHODS:A total of 230 Kazakh patients with coronary heart disease evidenced by coronary arteriography between December 2012 and July 2014 were recruited, and another 478 Kazak controls were free from coronary artery disease with normal angiograms. Real-time fluorescence quantitative PCR assay was used to detect the rs1007888 polymorphisms of MIF gene. Alele and genotype distributions of the rs1007888 polymorphism were compared between patients and controls. RESULTS AND CONCLUSION:Distribution of genotypes in the two groups appeared to be in Hardy-Weinberg equilibrium (P> 0.05). The alele frequencies and genotypes of MIF-rs1007888 showed no significant difference between the two groups (P > 0.05). Therefore, the genetic variation of rs1007888 in MIF gene is not associated with coronary heart disease in the Kazakhs of China.

Objective To study the effects of recruitment maneuver (RM) strategy on respiratory mechanics and extravascular lung water index (EVLWI) in patients with ARDS. Method Thirty patients with ARDS were randomly divided into RM group and non-RM group. In the RM group, the patients were stabilized with basic mechanical ventilation support for 30 minutes, and then the RM was carried out and repeated once every 12 hous for 3 days. In the non-RM group, patients were supported with mechanical ventilation without RM. The variables of oxygenation index (PaO2/FiO2), peak inspiration pressure (PIP), plateau pressure (Pplat), static pulmonary compliance (Cst) and EVLWI of patients in both groups were determined before treatment and 12 h,24 h, 48 h and 72 h after treatment, and were compared them between two groups. The hemodynamic changes were monitored before and after RM.One-way ANOVA, t -test and Fisher probabilities in 2/2 table were used to process the data. Results ( 1 ) The PaO2/FiO2 and Cst in two groups showed upward trend after treatment, but they were higher in RM group than those in non-RM group ( P ＜ 0. 05 ). The PIP and Pplat of two groups both had downward trend after treatment, but they were significantly lower in RM group than those in group non-RM (P ＜0.05). (2) The EVLWI of two groups showed downward trend after treatment ( P ＜ 0.05), and the differences were significant at all intervals (F: 22.392, 8.147, P ＜ 0.01). The EVLWIs in group RM were lower than those in group non-RM at the intervals of 12 h,24 h, 48 h and 72 h separately (P ＜0.05 or P ＜ 0.01). (3) There were transient hemodynamic changes occurred during RM, and compared with pre-RM, the changes were significantly different ( P＜ 0.01 ). Compared with pre-RM, the hemodynanic changes were not significantly different 120 seconds after the end of RM ( P ＞ 0.05). Conclusions RM could reduce the EVLWI, increase oxygenation and lung compliance.The effect of RM on hemodynamics was transient.

Objective To explore the mechanism and effect of miR-146a on alveolar macrophages and to observe the changes of miR-146a expression in the LPS-induced alveolar macrophages. Method NR8383 alveolar macrophages were divided into LPS-stimulated group and control group, and the cells of former group were treated with LPS ( 1 μg/mL) and then incubated for 3 h, 6 h and 12 h, respectively. The level of TNF-α in the supernatant of cells was assayed by using enzyme-linked immunosorbent assay (ELISA), and the expression of miR-146a of cells was detected by using Real-Time PCR (TaqMan probe).Statistical analysis carried out by using SPSS 13.0 software package in which One-way ANOVA and Student's t-test were used. Results Compared with control group, the levels of TNF-α in the supernatant of cells were significantly increased 3 h, 6 h and 12 h after LPS challenge (P ＜ 0.01 ). The expression of miR-146a increased 6 h and 12 h after LPS stimulation in NR8383 cells( P ＜0.01 ), and it had an upward tendency.Conclusions The expression of miR-146a in alveolar macrophages increases after LPS-stimulation. It hints miR-146a may be involved in the regulation of the inflammatory responses produced by alveolar macrophages.

OBJECTIVETo study the effect of ligustrazine on the migration of neuronal precursors (NPs) after focal cerebral ischemia in adult rats and explore its acting mechanism on recovery of function.

METHODSRat model of left middle cerebral artery occlusion (MCAO) was established by thread ligation. Ligustrazine 40 mg/kg was injected peritoneally once a day 2 h after modeling. On the 3rd, 7th, 14th and 21st day after operation, the migration of Doublecortin (DCX, the marker of NPs) in subventricular zone (SVZ) and the rostral migratory stream (RMS) were observed with immunohistochemistry.

RESULTSThe migration of DCX-positive cells in SVZ (abbrev. as migration below) through RMS into the olfactory bulb started from the 3rd day after ischemia, and lasted to the 21st day; the migration directly or through RMS into the ischemic penumbra of the adjacent striatum started on the 7th day, and increased significantly on the 14th day; and a few of DCX positive cells migrated through corpus callosum into the ischemic cortex on the 21st day. The migration was similar in the two groups in its pathway, but the extent in the ligustrazine group was more intensive.

CONCLUSIONLigustrazine could promote direct migration of NPs into the ischemic cerebral cortex and striatum, suggesting that it might play an important role in promoting self-recovery of brain function after ischemia through accelerating the migration of NPs.

Animals ; Anti-Inflammatory Agents, Non-Steroidal ; pharmacology ; Brain Ischemia ; physiopathology ; Cell Movement ; drug effects ; Immunohistochemistry ; Male ; Microtubule-Associated Proteins ; biosynthesis ; Neurons ; drug effects ; metabolism ; pathology ; Neuropeptides ; biosynthesis ; Pyrazines ; pharmacology ; Rats ; Rats, Sprague-Dawley

Objective:To investigate the effect and mechanism of exosomes derived from human-induced pluripotent mesenchymal stem cells (iMSC-Exos) on alveolar macrophages (AM) pyroptosis.Methods:The exosomes in the culture supernatant of human-induced pluripotent mesenchymal stem cells (iMSC) were extracted by rotating ultrafiltration, and the extracted exosomes were identified by transmission electron microscopy, Western blotting and high-resolution adjustable resistance pulse. The rat alveolar macrophage cells (NR8383 cells) were cultured in vitro and the logarithmic growth phase cells were divided into three groups: the control group was added with an equal volume of phosphate buffered saline (PBS) in the AM supernatant; in LPS/ATP group AM cells were stimulated with 500 μg/L LPS for 23 hours and then 5 mmol/L ATP was added for 1 hour to induce pyrolysis; iMSC-Exos group was incubated with AM and 100 mg/L iMSC-Exos for 3 hours before giving LPS and ATP. The cytotoxic activity was detected by cell counting kit-8 (CCK-8) and lactate dehydrogenase (LDH) analysis, the apoptosis and the expression of caspase-1 were observed by immunofluorescence, the levels of inflammatory factors interleukins (IL-1β and IL-18) released by AM were detected by enzyme linked immunosorbent assay (ELISA), the NOD-like receptor protein 3 (NLRP3) inflammasome pathway and the expression level of pyroptosis related protein gasdermin D (GSDMD) were detected by Western blotting. Results:The extracted exosomes were observed by transmission electron microscopy as round vesicles, expressing exosomal markers CD63 and CD9 showed by Western blotting, high-resolution adjustable resistance pulse showed the average diameter of the particles was 130 nm, and could be uptaken by AM. Compared with the control group, the cell activity decreased [(0.56±0.05)% vs. (1.06±0.07)%, P < 0.01], the release of necrotic substance LDH increased (U/L: 1 218.86±22.73 vs. 188.30±1.61, P < 0.01), the expression levels of inflammatory factors increased [IL-1β (ng/L): 958.91±32.78 vs. 194.63±5.14, IL-18 (ng/L): 870.89±21.86 vs. 288.85±24.48, both P < 0.01], and the apoptosis rate [(55.35±6.19)% vs. (12.01±1.32)%, P < 0.01] and caspase-1 expression (fluorescence intensity: 41.06±3.65 vs. 2.80±0.54, P < 0.01) elevated in the AM after LPS/ATP stimulation, suggesting that LPS combined with ATP successfully induced alveolar pyroptosis. Compared with the LPS/ATP group, AM pretreated with iMSC-Exos showed increased cell viability [(0.81±0.05)% vs. (0.56±0.05)%, P < 0.01], decreased LDH secretion (U/L: 535.05±42.55 vs. 1 218.86±22.73, P < 0.01), decreased expression of inflammatory factors [IL-1β (ng/L): 381.82±19.50 vs. 958.91±32.78, IL-18 (ng/L): 533.77±31.54 vs. 870.89±21.86, both P < 0.01], and decreased apoptosis rate [(19.74±2.96)% vs. (55.35±6.19)%, P < 0.01] and caspase-1 expression (fluorescence intensity: 12.16±1.31 vs. 41.06±3.65, P < 0.01). At the same time, the expression of NLRP3 inflammasome pathway [NLRP3 protein (NLRP3/β-actin): 0.62±0.06 vs. 1.89±0.11; cleaved caspase-1 protein (cleaved caspase-1/β-actin): 0.42±0.07 vs. 1.22±0.17, both P < 0.01] and pyrolysis-related protein was significantly inhibited [GSDMD protein (GSDMD/β-actin): 0.57±0.05 vs. 1.22±0.05, P < 0.01]. Conclusion:iMSC-Exos successfully reversed the AM pyroptosis and inflammatory factor expression induced by LPS/ATP, which may be due to the targeted inhibition of NLRP3 inflammasome pathway, suggesting that iMSC-Exos can exert anti-inflammatory effects by inhibiting the pyrolysis of AM.