Variations of p38 MAPK and sICAM-1 with therapeutic effect of different resuscitation fluids on severe traumatic patients / 中华创伤杂志(英文版)

<p><b>OBJECTIVE</b>To investigate the dynamic variation and action mechanism of sICAM-1 and p38 mitogen-activated protein kinases (MAPK) signal transduction in human severe trauma and resuscitation, as well as the effect of lactated Ringer's solution(LR), 7.5% sodium chloride solution(HS) and 20% albumin injection(ALB) on the incidence and mortality of multiple organ dysfunction syndrome (MODS).</p><p><b>METHODS</b>Seventy-two severe trauma patients (ISS score 16-43) were divided into ISS < or = 25 and ISS > 25 groups (each group was subdivided into LR, HS and ALB groups). ELISA was used to measure the concentration of sICAM-1. Western blot was used to measure the expression of p38 MAPK.</p><p><b>RESULTS</b>Compared with LR group, the transfusion volume needed for maintaining systolic blood pressure > or = 90 mm Hg was significantly decreased in HS and ALB groups (P < 0.05). Compared with the control group, the concentration of blood sICAM-1 and the expression of p38 MAPK was elevated from 4 to 48 hours after trauma in all experimental groups (P < 0.05-0.01). At 4, 12, and 24 hours, there was significant correlation between the expression of p38 MAPK and sICAM-1 (P < 0.01). Compared with LR group, sICAM-1 and p38 MAPK in HS and ALB groups were decreased (P < 0.05). sICAM-1 and p38 MAPK were significantly higher in the group of ISS > 25 than that of ISS < or = 25 (P < 0.05). MODS incidence and mortality were significantly higher in the group of ISS > 25 than that of ISS < or = 25 (P < 0.05). MODS incidence and mortality were lower in HS and ALB groups than LR group (P < 0.05).</p><p><b>CONCLUSIONS</b>The up-regulation of polymorphonuclear neutrophil-endotheliocytes (PMN-EC) adhesion may be due to the increased sICAM-1 expression during severe trauma. The up-regulation of sICAM-1 expression is correlated with the activation of p38 MAPK. During severe trauma, the levels of sICAM-1 and p38 MAPK, as well as the incidence and mortality of MODS are lower when HS and ALB are used than single lactated LR solution is used.</p>

Influence of human cytomegalovirus infection on cell cycle and replication licensing factor Cdt1 in human embryonic lung fibroblastic cells / 中国当代儿科杂志

<p><b>OBJECTIVE</b>To study the influence of human cytomegalovirus (HCMV) infection on cell cycle and the expression of replication licensing factor Cdt1 in human embryonic lung fibroblastic (HEL) cells and to explore the pathogenesis of HCMV infection.</p><p><b>METHODS</b>HEL cells were synchronized in the G0/G1 phase by the serum starvation method. The synchronized HEL cells were infected with HCMV, and those that were not subjected to HCMV infection were used as the control group. The HEL cells were harvested at 12, 24, 48, 72 and 96 hrs of HCMV infection. The cell cycle of HEL cells was detected by the flow cytometry. The expression of Cdt1 mRNA in HEL cells was determined by reverse transcription-polymerase chain reaction (RT-PCR).</p><p><b>RESULTS</b>The cells in the G1 phase in the control group was significantly more than in the HCMV-infected group 12 and 24 hrs after infection (P < 0.01). The expression of Cdt1 mRNA in the HCMV-infected group was significantly lower 12 and 24 hrs after infection but increased significantly 48 hrs after infection compared with the control group (P < 0.05). The expression of Cdt1 mRNA reached a peak at 12 hrs of infection in the control group, but at 48 hrs of infection in the HCMV-infected group, which markedly lagged behind the control group.</p><p><b>CONCLUSIONS</b>HCMV infection arrests the cell cycle of HEL cells at the G1 phase. HCMV infection makes Cdt1 expression delay. HCMV infection can interfere cell cycle of HEL cells possibly through affecting the expression of Cdt1.</p>