Seawater instillation-induced acute lung injury involves oxidative stress and apoptosis. Although hydrogen gas inhalation is reportedly protective in multiple types of lung injury, the effect of hydrogen gas inhalation on seawater instillation-induced acute lung injury remains unknown. This study investigated the effect of hydrogen gas on seawater instillation-induced acute lung injury and explored the mechanisms involved. Rabbits were randomly assigned to control, hydrogen (2 % hydrogen gas inhalation), seawater (3 mL/kg seawater instillation), and seawater + hydrogen (3 mL/kg seawater instillation + 2 % hydrogen gas inhalation) groups. Arterial partial oxygen pressure and lung wet/dry weight ratio were detected. Protein content in bronchoalveolar lavage fluid (BALF) and serum as well as tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6 levels were determined. Hematoxylin-eosin staining was used to monitor changes in lung specimens, and malondialdehyde (MDA) content and myeloperoxidase (MPO) activity were assayed. In addition, NF-E2-related factor (Nrf) 2 and heme oxygenase (HO)-1 mRNA and protein expression were measured, and apoptosis was assessed by measuring caspase-3 expression and using terminal deoxy-nucleotidyl transferase dUTP nick end-labeling (TUNEL) staining. Hydrogen gas inhalation markedly improved lung endothelial permeability and decreased both MDA content and MPO activity in lung tissue; these changes were associated with decreases in TNF-α, IL-1β, and IL-6 in BALF. Hydrogen gas also alleviated histopathological changes and cell apoptosis. Moreover, Nrf2 and HO-1 expressions were significantly activated and caspase-3 expression was inhibited. These results demonstrate that hydrogen gas inhalation attenuates seawater instillation-induced acute lung injury in rabbits and that the protective effects observed may be related to the activation of the Nrf2 pathway.

Objective This paper explores the effect of blood sample storage temperature and time on the erythrocyte sedimentation rate (ESR) by using the Weiss method. Methods Whole blood samples were collected from 80 patients and diluted 1:9 with sodium citrate solution. Each sample was split into two tubes. Using the Weiss method, ESR was tested within 1 h of collection, and one sample was placed at 4 °C and the other at room temperature (23 ± 2 °C). ESR was then measured at 2, 4, 6, 8, 12, and 24 h. The data were statistically analyzed with consideration for temperature and time. Results ESR decreased gradually over 6 h at room temperature, but the results were not statistically significant. Similarly, there was no significant difference in the decline of ESR within 8 h at 4 °C. However, ESR results decreased significantly after the samples were stored at room temperature for more than 6 h or at 4 °C for more than 8 h. ESR reduction was lower in the samples stored at 4 °C than in those stored at room temperature over the same time period. Conclusion Blood sample storage temperature and duration can affect the measurement of ESR using the Weiss method. ESR testing should be completed within 4 h of sample collection in clinical work.

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The aim of this study was to explore the value of serum amyloid A protein (SAA) and neutrophil-to-lymphocyte ratio (NLR) testing in the diagnosis and treatment of children with influenza A. Methods: Specimens were collected from 85 children with influenza A, 85 children with a bacterial infection, and 86 healthy children. The levels of SAA and C-reactive protein (CRP) were measured, and routine blood tests were performed. Results: The levels of SAA and CRP in the bacterial infection group were significantly higher than those in the influenza A group, and the levels in the influenza A group were higher than those in the healthy children. The NLR level in the influenza A group was not different from that in the bacterial infection group, but the NLR levels in the influenza A group and the bacterial infection group were higher than that in the healthy controls. The number of white blood cell (WBC) in the influenza A group was not different from that in healthy children, while the WBC counts in the control and bacterial infection groups were higher than that in the influenza A group. The distribution width of red blood cells in the bacterial infection group was higher than that in healthy controls. The receiver operating characteristic curve analysis showed that the area under the curve for the diagnoses of influenza A for SAA, NLR, and CRP was 0.806, 0.768, and 0.699, respectively. The sensitivity, specificity, positive predictive value, negative predictive value, and accuracy of SAA/NLR (SAA and NLR in the series) were 68.24%/76.47% (57.65%), 84.88%/72.09% (96.76%), 81.69%/73.03% (96.08%), 73.00%/75.61% (70.00%), and 76.61%/74.27% (77.78%), respectively. Conclusion: In the early diagnosis of children with influenza A, the values of SAA and NLR are high. Thus, they could be used for monitoring and efficacy evaluation during the course of the disease.