Wild type fragment of erythropoietin(Epo)3'-enhancer (W18) and its mutant type fragment (M18) were synthesized. Primary cultures of endothelial cells of different sources (ECs) and human umbilical venous endothelial cell line (HUVEC) as well as the primary culture of pulmonary artery smooth muscle cells (PASMC) were transfected with either W18 or M18. RT-PCR was performed to detect mRNA and investigate the effect of Epo3'-enhancer fragment on the hypoxia- induced gene expression in ECs. Electrophoretic mobility shift assay(EMSA) was used to test DNA-binding activity of extracted nuclear protein. ［3H］-TdR incorporation, MTT test and flow-cytometry were used to determine the proliferation of PASMC and the effect of Epo3'-enhancer fragment on it. The results showed as follows:(1)The OD value of COX-2 mRNA expressed in hypoxic rat aortic EC was 2.34±0.32, the OD values of COX-2 and VEGF mRNAs expressed in hypoxic EC of pulmonary microvasculature were 1.78±0.21 and 4.71±0.52, the OD value of TXS and ET-1 mRNAs in hypoxic HUVEC were 13.01±4.27 and 1.01±0.05, they were all higher than their counterpart normoxic group (P＜0.05). If the cells were pretransfected with W18, the OD values in these hypoxic groups became 1.28±0.25,0.77±0.09, 2.29±0.41, 4.88±1.05. and 0.51±0.15, respectively, just as low as those of the relevant normoxic groups; (2)The conditioned medium of hypoxic pulmonary artery endothelial cell (PAEC) caused proliferation of PASMC, the cpm values of ［3H］-TdR incorporation was 917.00±527.11, higher than that of normoxic control (P＜0.05). In addition, it was found by using flow-cytometry an increase in the percentage of cells of phases S and G2/M in PASMC incubated in hypoxic EC conditioned medium in comparison with normoxia group and group pretransfected with W18; (3)Hypoxia could induce proliferation of PASMC directly, transfection of W18 could decrease its effect. Their cpm values were 829.50±228.10 and 497.00±52.45, respectively(P＜0.05).The results of MTT test was similar; (4)The inducer of HIF-1, CoCl2 could increase the expression of COX-2 and TXS mRNA in HUVEC, which could also be inhibited by W18 but not by M18;(5)The HIF-1 DNA binding activity was found in hypoxic HUVEC in EMSA with　32　　　　P labeled W18, but not found with 　32　　　　P M18. These results suggest that there might be a common pathway in hypoxic responses of different cells, i.e. regulating the transcription of genes by binding of HIF-1 to a sequence similar to Epo3'-enhancer.

TXB_2 and 6-keto-PGF_(1?) levels of arterial and venous plasma in Wistar and4 Hilltep rats were measured to investigate the roles of TXA_2 and PGI_2 in the hypoxic pulmonary vasoconstriction(HPV) and responsiveness difference of pulmonary vessels to hypoxia between different strains of rats. The results showed that PGI_2 might play an important role in maintaining the low resistance of pulmonary circulation in these two strains of rats. TXA, increased during hypoxia might partially mediate HPV in Hilltop rats, on the contrary, PGI_2 augmented during hypoxia might modulate HPV in Wistar rats. This might be the major methanism responsible for the more intensive responsiveness of pulmonary vessels to hypoxia in Hilltop than in Wistar rats.

Acute hypoxic pulmonary vasoconstriction (HPV) plays an important role in physiological regulation. The purpose of this study was to explore the effects of Ilexonin A on hemodynamics and HPV, and their relation to prostaglandins (PG_(?)) and leukotrienes (LT_(?)).The results show that the high pulmonary vascular resistance induced by Ilexonin A in normoxic rats may be partially caused by the increased LTs and have no relation to PGs. Ilexonin A may potentiate HPV at least by two ways: replacing the production of PGs (especially PGI_2) in hypoxic Wistar rats, and increasing LTs production.

The alteration of hypoxic pulmonary vasoconstriction (HPV) induced bycigarette smoking was studied in Wistar rats, piglets and in humans. The percentage changeof pulmonary vascular resistance (△PVR%) and the amplitude of the systolic wave inimpedance pneumorheogram (△H%) were used to estimate the strength of HPV. It was observed that immediately after acute cigarette smoking, HPV in rats was in-creased (△PVR% from 55. 0?15. 6% to 102. 3?12. 4%), which was mainly mediated byleukotrienes (LTs); whereas HPV in piglets was decreased (△PVR% from 65.2?12. 5%to 55.9?9. 8%), which was mainly mediated by ? adrenergic receptors, and HPV inhumans was also increased (△H% from 20. 6? 2. 6% to 31. 1?4. 1%), in which prostag.landins and leukotrienes may play the role of mediators. However, after one-month ciga- rette smoking, the HPV of rats was significantly lowered (△PVR% 11. 4?1. 6%). Anincrease in vasodilative prostaglandins synthesis and a decrease in leukotrienes synthesismight haye contributed to this alteration of HPV.

Investigation of the roles of prostaglandins(PGs) and leukotrienes(LTs) inthe changes of hemodynamics and hypoxic pulmonary vasoconstriction(HPV) induced bychronic cigarette smoking in Wistar rats.After exposure to either smoke or room air, rats were anesthetized, the changes ofhemodynamics and hypoxic pulmonary vasoconstriction were measured. Blood samplesdrawn through the carotid arterial cannula were analyzed with radioimmunoassay(RIA)for PGs and bioassay for LTs in plasma. The results showed that cigarette smoking for onemonth did not change the pulmonary arterial pressure nor the pulmonary vascularresistance(PVR) in rats, while the pressure response of pulmonary vessels to hypoxiawas reduced significantly, which could be abolished by indomethacin. Cigarette smokingcould increase the concentration of 6-Keto-PGF_1?but not that of TXB_2, in arterial plasma,during hypoxia and it reduced the plasma level of LTs as well. These results suggestedthat chronic cigarette smoking might have reduced HPV by two ways: i. e. increasing theptoduction of vasodilative PGs, especially PGI_2, and reducing LTs production duringhypoxia.

Alteration of intracellular free calcium during hypoxia was studied in cul-tured porcine pulmonary arterial endothelial cells. Intracellular free calcium was measuredwith the fluorescent prob, Fura-2/AM. It was found that hypoxia induced by bubbling N_2 to cells suspension increased intracellular free calcium of endothelial cells by 81?21%(n=8, P

0.05). ②Among 30 pilots with abnormal vestibular functions,19 were permanently grounded and 11 were permitted to return their flying station. 36 pilots returned to fly in 45 cases with normal vestibular functions. The permanently grounded rate had significant differences between the two groups with normal and abnormal vestibular functions. (P

Objective:To evaluate the therapeutical effects of diplopore puncture of tympanum and intratympanic administration(DPTIA) on patients with acute secretory otitis media(ASOM).Method:One hundred and forty -one cases with ASOM were divided into two groups randomly,with 69 cases(80 ears) in group A(experimental group) and 72 cases(84 ears) in group B(control group).Group A was treated with DPTIA combined with medication, group B was treated with haplopore puncture of tympanum combined with medication. All patients accepted 1 to 3 courses of treament,and were observed during the period of treatment and 3 months after treatment.Result:The factors (including gender, age, side of ailing ear, course of disease, air-bone gap in the pure tone average,and acoustic immitance type in ailing ear) which may impact the prognosis were matched in two groups prior treatment(P＞0.05). While there was a significant difference in the cure rate and the total effective rate respectively between two groups after treatment(P＜0.05).No adverse reaction or complication was seen.Conclusion:DPTIA is a safe, reliable and effective way to manage patients with ASOM.

OBJECTIVE: Exploring the clinical features of aviatic nasal diseases to provide references for medical evaluation, prevention and control measures in aircrew. METHOD: To analysis and summary 605 cases with 503 pilots of nasal diseases in aircrew during 1966 to 2013. RESULT: (1) There were 605 cases of aviatic nasal diseases, including 550 cases of general diseases and 55 cases of specific diseases. The general nasal diseases included 140 cases of anatomical abnormalities in nasal cavity type, 290 cases of inflammation in nasal cavity, 73 cases of allergy type, 47 cases of cyst and tumor type, and the specific nasal diseases were 55 cases of sinus barotrauma (SB). (2) The, constituent ratio of SB, which was happened in frontal sinus and /or maxillary sinus, was 95.55%. (3) The constituent ratio of cyst and tumor type in nasal cavity was easier causing to SB than anatomical abnormalities, inflammation, allergy disease in nasal cavity (P < 0.05). (4) The grounded constituent ratio of secondary SB was higher than anatomical abnormalities, inflammation, allergy, cyst and tumor disease in nasal cavity (P < 0.05). (5) The ways of hypobaric chamber tests were different for the kinds of aircrew. The qualified adjustment function of sinuses for barometric pressure was an essential condition for aircrew to continue flying. (6) The key point for the treatment of aviatic nasal diseases was to remove pathological change in nasal cavity and sinus and restore sinus ostium patency. The key point for the medical evaluation was to restore normal sinus pressure balance function. CONCLUSION The key point of medical evaluation about aviatic nasal diseases is to assess the sinus pressure balance function in hypobaric chamber tests. Normative treatment and medical evaluation can effectively avoid flight accidents and improve the attendance rate for aircrew.
Aerospace Medicine ; Barotrauma ; Cysts ; Frontal Sinus ; pathology ; Humans ; Hypersensitivity ; Maxillary Sinus ; pathology ; Nasal Cavity ; pathology ; Nose Diseases ; epidemiology ; prevention & control ; Paranasal Sinuses ; pathology

Objective To investigate whether recombinant human endostatin can create a time window of vascular normalization prior to vascular pruning to alleviate hypoxia in Lewis lung carcinoma in mice. Methods Kinetic changes in morphology of tumor vasculature in response to recombinant human endostatin were detected under a confocal microscope with immunofluorescent staining in Lewis lung carcinomas in mice. The hypoxic cell fraction of different time was assessed with immunohistochemical staining . Effects on tumor growth were monitored as indicated in the growth curve of tumors . Results Compared with the control group vascularity of the tumors was reduced over time by recombinant human endostatin treatment and significantly regressed for 9 days. During the treatment, pericyte coverage increased at day 3, increased markedly at day 5, and fell again at day 7. The vascular basement membrane was thin and closely associated with endothelial cells after recombinant human endostatin treatment, but appeared thickened, loosely associated with endothelial cells in control tumors. The decrease in hypoxic cell fraction at day 5 after treatment was also found. Tumor growth was not accelerated 5 days after recombinant human endostatin treatment. Conclusions Recombinant human endostatin can normalize tumor vasculature within day 3 to 7, leading to improved tumor oxygenation. The results provide important experimental basis for combining recombinant human endostatin with radiation therapy in human tumors.