Objective:To investigate the physiological changes of people when advancing rapidly to the plateau, and to evaluate the performance of high-altitude simulation device.Methods:A total of 24 healthy volunteers were randomly divided into 4 groups with 6 individuals in each by the random number table method. The high-altitude simulation device was used to simulate the plateau in two stages. The first stage simulated an altitude of 3 500 m (equivalent to high altitude), and the second stage was performed after an interval of 24 hours from the first stage, which simulated an altitude of 5 000 m (equivalent to ultra-high altitude). During the two stages, for blood routine and blood gas analysis, blood samples were taken before entering the chamber of each stage, and at the simulated altitudes of 3 500 and 5 000 m in the chamber. Furthermore, ECG tests were also conducted before and after entering the chamber. In the case of cardiac abnormality, the cardiac enzyme test would be carried out. Meanwhile, one volunteer in each group was under ECG monitoring.Results:As the simulated altitude increased, the volunteers’ pulse rates increased gradually, while their saturation of periferal oxygen(SpO 2) decreased gradually. Comparing the pulse rate and SpO 2 at 3 500 m with those before entering the chamber, and comparing the pulse rate and SpO 2 at 5 000 m with those before entering the chamber; all the differences were statistically significant ( P<0.05, or P<0.01). The blood routine tests demonstrated a significant increase in the total counts of red blood cells, hemoglobin, platelets and white blood cells and other contents at the first stage, i. e., 3 500 m; and the differences were statistically significant compared with those before entering the chamber ( P<0.05, or P<0.01). Furthermore, the pH values increased gradually, whereas arterial partial pressure of oxygen (PaO 2), oxygen saturation (SaO 2), and arterial partial pressure of carbon dioxide (PaCO 2) decreased gradually. The significant decrease in HCO 3- showed at 5, 000 m, and the differences were statistically significant compared with those before entering the chamber ( P<0.05, or P<0.01). Conclusion:The plateau simulation can reflect physiological changes of the human body after advancing rapidly to the plateau under the premise of ensuring safety. It has laid a foundation for the further implementation of plateau acclimatization on plain area.

Objective:To investigate the physiological changes of people when advancing rapidly to the plateau, and to evaluate the performance of high-altitude simulation device.Methods:A total of 24 healthy volunteers were randomly divided into 4 groups with 6 individuals in each by the random number table method. The high-altitude simulation device was used to simulate the plateau in two stages. The first stage simulated an altitude of 3 500 m (equivalent to high altitude), and the second stage was performed after an interval of 24 hours from the first stage, which simulated an altitude of 5 000 m (equivalent to ultra-high altitude). During the two stages, for blood routine and blood gas analysis, blood samples were taken before entering the chamber of each stage, and at the simulated altitudes of 3 500 and 5 000 m in the chamber. Furthermore, ECG tests were also conducted before and after entering the chamber. In the case of cardiac abnormality, the cardiac enzyme test would be carried out. Meanwhile, one volunteer in each group was under ECG monitoring.Results:As the simulated altitude increased, the volunteers’ pulse rates increased gradually, while their saturation of periferal oxygen(SpO 2) decreased gradually. Comparing the pulse rate and SpO 2 at 3 500 m with those before entering the chamber, and comparing the pulse rate and SpO 2 at 5 000 m with those before entering the chamber; all the differences were statistically significant ( P<0.05, or P<0.01). The blood routine tests demonstrated a significant increase in the total counts of red blood cells, hemoglobin, platelets and white blood cells and other contents at the first stage, i. e., 3 500 m; and the differences were statistically significant compared with those before entering the chamber ( P<0.05, or P<0.01). Furthermore, the pH values increased gradually, whereas arterial partial pressure of oxygen (PaO 2), oxygen saturation (SaO 2), and arterial partial pressure of carbon dioxide (PaCO 2) decreased gradually. The significant decrease in HCO 3- showed at 5, 000 m, and the differences were statistically significant compared with those before entering the chamber ( P<0.05, or P<0.01). Conclusion:The plateau simulation can reflect physiological changes of the human body after advancing rapidly to the plateau under the premise of ensuring safety. It has laid a foundation for the further implementation of plateau acclimatization on plain area.

The aim of the present study is to investigate the effects of Vam3 which is one of the dihydroxystilbene compounds on expressions of ICAM-1 in the lungs of OVA-induced asthmatic mice and the mechanisms of anti-airway inflammation. Balb/c mice were challenged with OVA inhalation. Lung tissues were stained with Mayer's hematoxylin and eosin for histopathologic examination. The expression of ICAM-1 in the lungs of mice was analyzed by Western blotting and immunohistochemistry method. The NF-kappaB activities were detected by NF-kappaB-luc reporter genetic transient transfection method. The activities of MMP-9 induced by LPS, TNF-alpha and PMA in THP-1 cells were determined by gelatin zymography method. The results showed that Vam3 could inhibit the expression of ICAM-1 in the OVA-induced mouse model. In addition, Vam3 could significantly suppress the activities of NF-kappaB in A549 cells and MMP-9 in THP-1 cells induced by LPS, TNF-alpha and PMA. These results suggested that Vam3 could alleviate the asthmatic inflammation by decreasing ICAM-1 expression in asthmatic mice, down regulating NF-kappaB and MMP-9 activities. Compound Vam3 showed inhibitory effects on inflammatory signal pathways involved in asthma.

Microarray analysis revealed that the expression of ferric reductase (FRP1) can be regulated by the Riml01 protein. In order to find new transcriptional regulatory element in the promoter of FRP1, we analyzed the 1000 bp sequence upstream of ATG to find 2 potential Riml01p binding sites. We generated site-specific mutations in each of the two sites and fused these mutated promoters to LacZ. Then the promoter-LacZ fusion construct was recombinant into wild type and riml01-/- strains for beta-galactosidase assay. The results revealed that the FRP1 was up-regulated in alkaline pH and this was caused by iron starvation. The -650 site, not the -160 site, had an important role in FRP1 Riml01p-dependent expression. We conclude that Riml01p may interact with the -650 binding site of the promoter to regulate the FRP1 expression.
Candida albicans ; enzymology ; genetics ; DNA-Binding Proteins ; genetics ; FMN Reductase ; genetics ; Fungal Proteins ; genetics ; Mutagenesis, Site-Directed ; Promoter Regions, Genetic ; genetics