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Wang Z.,Institute of Naval Medical Research | Yang Y.,Institute of Naval Medical Research | Wang H.,Institute of Naval Medical Research | Wang Y.,Institute of Naval Medical Research | And 2 more authors.
He Jishu/Nuclear Techniques

A strippable film of polyvinyl alcohol (PVA) for decontamination of radioactive dusts on stainless steel (SS) device surface was developed by investigating the film-stripping ability from the SS surface and the contamination-removal efficiency of the films of various preparation parameters. They include PVA concentration of the film-making solution, and amounts of EDTA-Na-Ca as complexing agent, CMC-2Na as thickening agent, PEG-200 as plasticizer, nmCaCO3 as surfactant, and 1.85 mol/L HCl. The PVA film, which can be dried in 8 h, is capable of removing over 80% of surface contamination of 90Sr at 0.02-0.20 Bq/cm2. Source

Bao X.-C.,Institute of Naval Medical Research | Chen H.,Health Testing Center | Fang Y.-Q.,Institute of Naval Medical Research | Yuan H.-R.,Institute of Naval Medical Research | And 3 more authors.
Respiratory Physiology and Neurobiology

Inflammation and platelet activation are critical phenomena in the setting of decompression sickness. Clopidogrel (Clo) inhibits platelet activation and may also reduce inflammation. The goal of this study was to investigate if Clo had a protective role in decompression sickness (DCS) through anti-inflammation way. Male Sprague-Dawley rats (. n=. 111) were assigned to three groups: control. +. vehicle group, DCS. +. vehicle, DCS. +. Clo group. The experimental group received 50. mg/kg of Clo or vehicle for 3 days, then compressed to 1,600. kPa (150. msw) in 28. s, maintained at 150. msw for 242. s and decompressed to surface at 3. m/s. In a control experiment, rats were also treated with vehicle for 3 days and maintained at atmospheric pressure for an equivalent period of time. Clinical assessment took place over a period of 30. min after surfacing. At the end, blood samples were collected for blood cells counts and cytokine detection. The pathology and the wet/dry ratio of lung tissues, immunohistochemical detection of lung tissue CD41 expression, the numbers of P-selectin positive platelets and platelet-leukocyte conjugates in blood were tested. We found that Clo significantly reduced the DCS mortality risk (mortality rate: 11/45 with Clo vs. 28/46 in the untreated group, P<. 0.01). Clo reduced the lung injury, the wet/dry ratio of lung, the accumulation of platelet and leukocyte in lung, the fall in platelet count, the WBC count, the numbers of activated platelets and platelet-leukocyte complexes in peripheral blood. It was concluded that Clo can play a protective role in decompression sickness through reducing post-decompression platelet activation and inflammatory process. © 2015 Elsevier B.V. Source

Bao X.-C.,Institute of Naval Medical Research | Fang Y.-Q.,Institute of Naval Medical Research | You P.,Institute of Naval Medical Research | Zhang S.,Institute of Naval Medical Research | Ma J.,Institute of Naval Medical Research
Experimental Lung Research

Recent studies have demonstrated that peroxisome proliferator-activated receptor-beta/delta (PPAR-β/δ) has a protective effect during lung injury induced by bleomycin and polymicrobial sepsis, but its function in pulmonary oxygen toxicity is unknown. In this study, we used GW0742, a PPAR-β/δ agonist, and GSK0660, a PPAR-β/δ antagonist, to test the role of PPAR-β/δ in lung injury due to hyperbaric oxygen (HBO2) exposure. Lung injury was induced in rats by HBO2 exposure (2.3 ATA, 100%O2, 8 hours). Sixty male Sprague-Dawley rats were randomly divided into 6 groups: air+vehicle, air+GW0742, air+GSK0660, HBO2+vehicle, HBO2+GW0742, and HBO2+GSK0660. Rats were injected with vehicle or GW0742 (0.3 mg/kg, i.p.) or GSK0660 (1 mg/kg, i.p.) at 1 hour, 6 hours, and 12 hours before either air or oxygen exposure. Administration of GW0742 to rats exposed to HBO2 significantly reduced the observed lung injury, extravascular lung water, total protein levels in bronchoalveolar lavage fluid, and the levels of iNOS and nNOS in the lungs when compared to untreated rats exposed to HBO2. Treatment of rats with GSK0660 exacerbated lung injury and elevated the levels of nNOS and eNOS in the lungs. In addition, nNOS and eNOS knock-out mice were examined. The results indicated that after HBO2 exposure, the lung injury was obviously decreased in the nNOS-/-+GSK0660 mice compared to the wild-type +GSK0660 mice; furthermore, administration of GSK0660 significantly elevated the lung injury in the eNOS-/- mice. Collectively, these data indicate that PPAR-β/δ activation can protect against pulmonary oxygen toxicity in the lungs of rats through changes in the expression of NOS. © 2014 Informa Healthcare USA, Inc. Source

Bao X.-C.,Institute of Naval Medical Research | Fang Y.-Q.,Institute of Naval Medical Research | You P.,Institute of Naval Medical Research | Zhang S.,Institute of Naval Medical Research | Ma J.,Institute of Naval Medical Research
Respiratory Physiology and Neurobiology

Peroxisome proliferator-activated receptor (PPAR)-β/δ is a transcription factor that belongs to the PPAR family, but the role of PPAR-β/δ in acute lung injury (ALI) induced by hyperbaric oxygen is unknown. In this study we investigated if PPAR-β/δ activation protects from hyperoxia-induced ALI in a rat model. ALI was induced by prolonged hyperbaric oxygen (HBO2) (2.3ATA, 100% O2) for 8h. Administration of PPAR-β/δ agonist GW0742 (0.3mg/kg, i.p.) at 1 and 6h prior to HBO2 exposure significantly reduced the (1) lung injury, (2) proinflammatory cytokines (TNF-α, IL-1β, IL-6), (3) apoptosis (Bax/Bcl-2, cleaved-caspase-3 and TUNEL), (4) nuclear factor (NF)-κB expression level and DNA binding activity in the nucleus, and (5) extracellular signal-regulated kinase (ERK)1/2 phosphorylation and markedly elevated (6) superoxide dismutase and glutathione peroxidase activities as well as (7) IκB expression. However, administration of the PPAR-β/δ antagonist GSK0660 abolished these protective effects. These findings indicate that activation of PPAR-β/δ ameliorates hyperoxia-induced ALI in rats by up-regulating antioxidant enzyme activity as well as suppressing inflammation and apoptosis. © 2014 Elsevier B.V. Source

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