Objective To investigate the triggering receptor expressed on myeloid cells-1(TREM-1) of cord blood leukocytes in neonates and the transcription level of mRNA, and analyze its promoting function of inflammatory cytokine secretion. Methods During the period from September 2013 to March 2014, cord blood was collected from 20 term neonates at the time of birth, and peripheral blood was collected from 20 healthy adults. The expression of TREM-1 and TREM-1 mRNA on leukocytes was observed using flow cytometry and real-time reverse transeription-polymerase chain reaction, respectively. After the whole cord blood was stimulated by lipopolysaccharide (LPS) or LP17 plus LPS, the contents of interleukin (IL)-6, tumor necrosis factor-α (TNF-α), IL-8 and soluble TREM-1 (sTREM-1) in the supernatant were analyzed by enzyme linked immunosorbent assay. The statistical significance was determined using the one-way ANOVA test, t test, q test and Pearson correlation coefficient. Results The mean fluorescence intensity of TREM-1 on leukocytes of newborns was not different compared with healthy adults (P>0.05), while the percentage of TREM-1 positive on polymorphonuclear cells was lower than that of healthy adults [(82.3±7.1)% vs (98.6±4.8)%, P<0.05]. The level of TREM-1 mRNA in newborns was lower than in healthy adults (1.16±0.13 vs 1.63±0.24, t=7.714, P<0.01). The LPS treatment significantly increased sTREM-1 in newborn whole blood compared with the control treatment [(156.7±36.3) vs (34.6±6.1) pg/ml, t=13.623, P<0.01]. The concentration of IL-6, TNF-αand IL-8 decreased significantly when TREM-1 was blocked by LP17. In addition, the concentration of sTREM-1 showed a positive correlation with the levels of TNF-α(r=0.519, P<0.05), IL-6 (r=0.507, P<0.05) and IL-8 (r=0.538, P<0.05). Conclusions Healthy newborns exhibit expression of TREM-1 on monocytes similar to healthy adults, and most PMNs express TREM-1 at the newborn stage. Blocking the TREM-1 signal transduction pathway may reduce inflammatory responses of neonate leukocytes.

Objective To observe whether pressure boost could induce changes in intracardiac pressures,and also to investigate the mechanism involved.Methods Seventeen healthy volunteers [13 males and 4 females,with an age range of 25.76 ± 5.16 years,and average age of 18-34] were recruited for the study.Without the knowledge of the examiners and examinees about the purpose of the research,they entered the hyperbaric chamber.The examiners detect the intraocular pressures (IOP) of the examinees with the Japanese NIDEK NT-2000 non-contact tonometer under the following conditions:(1) baseline intraocular pressures at rest.(2) during the stay at atmospheric pressure for 30 min without breathing pure oxygen; after breathing pure oxygen for 10 min at atmospheric pressure.(3) compression to a pressure of 60 kPa at a rate of 2.0 kPa/s without breathing pure oxygen; (4) during the stay at the pressure of 60 kPa for 30 min without breathing pure oxygen ; (5) after decompression to 0 kPa pressure,also without breathing pure oxygen.Results Average intraocular pressures measured during their stay at atmospheric pressure for 30 min without breathing pure oxygen,after breathing pure oxygen for 10 min at atmospheric pressure and after decompression to 0 kPa pressure without breathing pure oxygen were (13.57 ±3.04),(13.86 ± 3.16) and (13.33 ± 3.12) mmHg respectively.No statistical significance could be seen in measured data,as compared with that of the baseline intraocular pressures [(13.48 ± 2.87) mmHg] (P ＞ 0.05).Average intraocular pressures measured after they were compressed to 60 kPa without breathing pure oxygen and during their stay at 60 kPa for 30 min without breathing pure oxygen were (16.06 ±2.48) and (15.65 ± 2.54) mmHg respectively,and statistical difference could be seen,when compared with that of the baseline intraocular pressures(P ＞ 0.01).Conclusions When there was a pressure boost,most people would display elevated IOP due to poor response to pressure,only a few people would experience IOP drop also due to poor response to pressure and IOP of still a few people would remain basically unchanged.

Objective To observe whether pressure boost could induce changes in intracardiac pressures,and also to investigate the mechanism involved.Methods Seventeen healthy volunteers [13 males and 4 females,with an age range of 25.76 ± 5.16 years,and average age of 18-34] were recruited for the study.Without the knowledge of the examiners and examinees about the purpose of the research,they entered the hyperbaric chamber.The examiners detect the intraocular pressures (IOP) of the examinees with the Japanese NIDEK NT-2000 non-contact tonometer under the following conditions:(1) baseline intraocular pressures at rest.(2) during the stay at atmospheric pressure for 30 min without breathing pure oxygen; after breathing pure oxygen for 10 min at atmospheric pressure.(3) compression to a pressure of 60 kPa at a rate of 2.0 kPa/s without breathing pure oxygen; (4) during the stay at the pressure of 60 kPa for 30 min without breathing pure oxygen ; (5) after decompression to 0 kPa pressure,also without breathing pure oxygen.Results Average intraocular pressures measured during their stay at atmospheric pressure for 30 min without breathing pure oxygen,after breathing pure oxygen for 10 min at atmospheric pressure and after decompression to 0 kPa pressure without breathing pure oxygen were (13.57 ±3.04),(13.86 ± 3.16) and (13.33 ± 3.12) mmHg respectively.No statistical significance could be seen in measured data,as compared with that of the baseline intraocular pressures [(13.48 ± 2.87) mmHg] (P ＞ 0.05).Average intraocular pressures measured after they were compressed to 60 kPa without breathing pure oxygen and during their stay at 60 kPa for 30 min without breathing pure oxygen were (16.06 ±2.48) and (15.65 ± 2.54) mmHg respectively,and statistical difference could be seen,when compared with that of the baseline intraocular pressures(P ＞ 0.01).Conclusions When there was a pressure boost,most people would display elevated IOP due to poor response to pressure,only a few people would experience IOP drop also due to poor response to pressure and IOP of still a few people would remain basically unchanged.