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This study examined biological characteristics, liquid fermentation, and cultivation of Fomitopsis pinicola. A single-factor test concluded that the optimal carbon and nitrogen sources for mycelial growth were soluble starch and yeast paste; the optimal culture temperature was 31°C, and the optimal pH was 6.0. The orthogonal experiment indicated that the optimal formula for mycelial culture was 25 g soluble starch, 2 g yeast extract, 1 g KH2PO4, and 1.5 g MgSO4 added to 1 L water. The optimal conditions for liquid fermentation culture consisted of the following: a loading volume 90 mL, inoculation volume 30 mL, and rotation speed 160 rpm. The optimal substrate formula for domestic culture was 20% corn cob, 30% sawdust, 20% wheat bran, 25% cotton seed shell, 3% corn meal, 1% gypsum, and 1% lime, which produced the highest yield of fruiting bodies. The results provided basic data for deep liquid fermentation culture and recommendations for the further development and utilization of F. pinicola.

Background We previously reported that maternal alcohol use significantly increases the risk of sepsis in premature and term newborns. In the mouse, fetal ethanol exposure results in an immunosuppressed phenotype for the alveolar macrophage (AM) and decreases bacterial phagocytosis. In pregnant mice, ethanol decreased AM zinc homeostasis, which contributed to immunosuppression and impaired AM phagocytosis. In this study, we explored whether ethanol-induced zinc insufficiency extended to the pup AMs and contributed to immunosuppression and exacerbated viral lung infections. Methods C57BL/6 female mice were fed a liquid diet with 25% ethanol-derived calories or pair-fed a control diet with 25% of calories as maltose-dextrin. Some pup AMs were treated in vitro with zinc acetate before measuring zinc pools or transporter expression and bacteria phagocytosis. Some dams were fed additional zinc supplements in the ethanol or control diets, and then we assessed pup AM zinc pools, zinc transporters, and the immunosuppressant TGFβ1. On postnatal day 10, some pups were given intranasal saline or respiratory syncytial virus (RSV), and then AM RSV phagocytosis and the RSV burden in the airway lining fluid were assessed. Results Fetal ethanol exposure decreased pup AM zinc pools, zinc transporter expression, and bacterial clearance, but in vitro zinc treatments reversed these alterations. In addition, the expected ethanol-induced increase in TGFβ1 and immunosuppression were associated with decreased RSV phagocytosis and exacerbated RSV infections. However, additional maternal zinc supplements blocked the ethanol-induced perturbations in the pup AM zinc homeostasis and TGFβ1 immunosuppression, thereby improving RSV phagocytosis and attenuating the RSV burden in the lung. Conclusion These studies suggest that, despite normal maternal dietary zinc intake, in utero alcohol exposure results in zinc insufficiency, which contributes to compromised neonatal AM immune functions, thereby increasing the risk of bacterial and viral infections.

Inactivated foot-and-mouth disease virus (FMDV) vaccines have been used widely to control foot-and-mouth disease (FMD). However, the virions (146S) of this virus are easily dissociated into pentamer subunits (12S), which limits the immune protective efficacy of inactivated vaccines when the temperature is higher than 30 °C. A cold-chain system can maintain the quality of the vaccines, but such systems are usually not reliable in limited-resource settings. Thus, it is imperative to improve the thermostability of vaccine strains to guarantee the quality of the vaccines. In this study, four recombinant FMDV strains containing single or multiple amino acid substitutions in the structural proteins were rescued using a previously constructed FMDV type O full-length infectious clone (pO/DY-VP1). We found that single or multiple amino acid substitutions in the structural proteins affected viral replication to different degrees. Furthermore, the heat and acid stability of the recombinant viruses was significantly increased when compared with the parental virus. Three thermally stable recombinant viruses (rHN/DY-VP1Y2098F, rHN/DY-VP1V2090A-S2093H, and rHN/DY-VP1V2090A-S2093H-Y2098F) were prepared as inactivated vaccines to immunize pigs. Blood samples were collected every week to prepare sera, and a virus neutralization test showed that the substitutions S2093H and Y2098F, separately or in combination, did not affect the immunogenicity of the virus, but the Y2098F mutation increased the thermostability significantly (p < 0.05). Therefore, the rHN/DY-VP1Y2098F mutant should be considered for use in future vaccines.

Based on the establishment of analytical method of ultra-high performance liquid chromatography-tandem mass spectrometry fingerprint and obtaining pharmacodynamic information of the effects on IL-4...

Phosphates can cost-effectively decrease the mobility of Pb in contaminated soils. However, Pb always coexists with other metals in soil, their competitive reactions with phosphates have not been tested. In this study, the abilities of KH2PO4, K2HPO4, and K3PO4 to stabilize Pb, Zn, and Cd in soils contaminated with a single metal or a ternary metal for different phosphorus/metal molar ratios were investigated. Results indicated that the stabilization efficiency of KH2PO4, K2HPO4, and K3PO4 for Pb, Zn, and Cd in single metal contaminated soil (P/M ratio 0.6) was 96.00%–98.74%, 33.76%–47.81%, and 9.50%–55.79%, respectively. Competitive stabilization occurred in the ternary system, Pb exhibited a strong competition, the stabilization efficiency of Zn and Cd reduced by 23.50%–31.64%, and 7.10%–39.26%, respectively. Pyromorphite and amorphous lead phosphate formed with excess KH2PO4 or K2HPO4 addition, while K3PO4 resulted in the formation of a hydroxypyromorphite precipitate. Amorphous Zn and Cd phosphates and hydroxides were the primary products. The immobilization rate of Zn and Cd depends on pH, and increased significantly in response to the excess phosphate application. This approach provides insight into phosphate-induced differences in stabilization efficiency in soils contaminated with multiple metals, which is of theoretical and engineering significance.

Aims: (a) Establish the minimum number of weeks of chronic ethanol ingestion needed to perturb zinc homeostasis, (b) Examine intracellular zinc status in the alveolar macrophages (AMs) when ethanol ingestion is combined with pregnancy, (c) Investigate whether in vitro zinc treatment reverses the effects of ethanol ingestion on the AM. Methods: C57BL/6 female mice were fed a liquid diet (±25% ethanol-derived calories) during preconception and pregnancy. The control group was pair-fed to the ethanol group. In the isolated AMs, we measured intracellular AM zinc levels, zinc transporter expression, alternative activation and phagocytic index. Zinc acetate was added to some cells prior to analysis. Results: Intracellular zinc levels in the AM decreased within 3 weeks of ethanol ingestion. After ethanol ingestion prior to and during pregnancy, zinc transporter expression and intracellular zinc levels were decreased in the AMs when compared with controls. Bacterial clearance was decreased because the AMs were alternatively activated. In vitro additions of zinc reversed these effects of ethanol. Conclusion: Ethanol ingestion prior to and during pregnancy perturbed AM zinc balance resulting in impaired bacterial clearance, but these effects were ameliorated by in vitro zinc treatments.

Background In 2014–2015, 242 individuals aged 2–89 years were newly diagnosed with human immunodeficiency virus type 1 (HIV-1) in Roka, a rural commune in Cambodia. A case-control study attributed the outbreak to unsafe injections. We aimed to reconstruct the likely transmission history of the outbreak. Methods We assessed in 209 (86.4%) HIV-infected cases the presence of hepatitis C virus (HCV) and hepatitis B virus (HBV). We identified recent infections using antibody (Ab) avidity testing for HIV and HCV. We performed amplification, sequencing, and evolutionary phylogenetic analyses of viral strains. Geographical coordinates and parenteral exposure through medical services provided by an unlicensed healthcare practitioner were obtained from 193 cases and 1499 controls during interviews. Results Cases were coinfected with HCV (78.5%) and HBV (12.9%). We identified 79 (37.8%) recent ( Conclusions Unsafe injections in Cambodia most likely led to an explosive iatrogenic spreading of HIV, associated with a long-standing and more genetically diverse HCV propagation.

Bauxite residue neutralization is intended to open opportunities for revegetation and reuse of the residue. Ferrous sulfate (FS) and nitrohumic acid (NA) were two kinds of materials studied for pH reduction of the residue from 10.6 to 8.3 and 8.1, respectively. The effects of FS and NA on the leaching of metals from a combined bauxite residue were investigated by using sequential and multiple extraction procedures. Neutralization with FS and NA restricted the leaching of Al, V, and Pb from the residue but promoted the leaching of Fe, Cu, Mn, and Ni, consistent with the changes in the potentially mobile fractions. With the exceptions of Pb and Ni, leaching of metals increased during a 10-day extraction period. However, the maximum leaching of Al, V, Pb, Fe, Cu, Mn, and Ni from neutralized bauxite residue were 0.46 mg/L, 59.3, 12.9, 167, 95.3, 15.5, and 14.5 μg/L, respectively, which were under the corresponding limits in the National Standard (GB/T 14848-93). Although it is necessary to consider the continued leaching of metals during neutralization, both maximum and accumulation leaching concentrations of metals from a combined bauxite residue were too low to pose a potential environmental risk.

A new method was established to determine short-chain chloroparaffins (SCCPs) in synthetic surfacing layers used in sports and diluents by solid-phase extraction (SPE) coupled with gas chromatography-negative chemical ionization-mass spectrometry (GC-NCI-MS). The analysis conditions for gas chromatography and mass spectrometry were optimized. Then, the samples were extracted by ultrasonication, purified on a Florisil SPE column, monitored in the selective ion monitoring (SIM) scanning mode, and quantified by the external standard method. With this method, a good linear relationship was found over a wide mass concentration range from 0.0501 to 100.17 mg/L, with a linear correlation coefficient (R2) of 0.9995. The detection limit for SCCPs by this method was found to be as low as 0.50 μg/g (i. e. 0.000050%) and the average recoveries for SCCPs spiked in the blank samples varied from 83.2% to 96.3% with relative standard deviations (RSDs) of 1.56%-6.02%. Ten batches of samples were tested and the contents of SCCPs detected in each batch were in the range from 0.016% to 0.55%, which agrees well the European Union limitation requirement for SCCPs. Thus, this method is suitable for qualitative and quantitative analyses of SCCPs in synthetic surfacing layers used in sports and diluents.

We have previously demonstrated that chronic alcohol exposure decreases glutathione in the alveolar space. Although alcohol use is associated with decreased alveolar macrophage function, the mechanism by which alcohol impairs macrophage phagocytosis is unknown. In the current study, we examined the possibility that ethanol-induced alveolar macrophage dysfunction was secondary to decreased glutathione and subsequent chronic oxidative stress in the alveolar space. After 6 wk of ethanol ingestion, oxidant stress in the alveolar macrophages was evidenced by a 30-mV oxidation of the GSH/GSSG redox potential ( P ≤ 0.05). For control macrophages, ∼80% internalized fluorescent Staphylococcus aureus were added in vitro. In contrast, only 20% of the macrophages from the ethanol-fed rats were able to bind and internalize fluorescent S. aureus. This ethanol-induced decreased capacity for phagocytosis was paralleled by increased apoptosis. When added to the ethanol diet, the glutathione precursors procysteine or N-acetyl cysteine normalized glutathione and oxidant stress in the epithelial lining fluid as well as the alveolar macrophages to control values. This attenuation of oxidant stress was associated with normalization of macrophage phagocytosis and viability. These results suggested that decreased glutathione availability in the alcoholic lung contribute to alveolar macrophage dysfunction via oxidative stress, resulting in not only decreased function but decreased viability.

Our understanding of the intrinsic effects of cystic fibrosis (CF) transmembrane conductance regulator ( cftr ) deletion on resident neonatal alveolar macrophage (AM) remains limited. We previously demonstrated that diminished glutathione (GSH) or excessive AM transforming growth factor beta one (TGF β 1) contributes to AM dysfunction in a variety of disease states. In this study, using a gut‐corrected cftr neonatal knockout (KO) mouse model and a siRNA‐manipulated macrophage‐like cell line (THP‐1 cell), we hypothesized (1) that cftr mutation alone increases neonatal AM oxidant stress and cellular TGF β 1 signaling via altered GSH, thereby impairing cellular function, and (2) that exogenous GSH attenuates AM alterations and dysfunction in the KO AM. In neonatal KO mice, the baseline bronchoalveolar lavage fluid demonstrated a near doubling in mixed disulfides ( P ≤ 0.05) and oxidized GSSG ( P ≤ 0.05) without concurrent inflammation compared to WT littermates. KO AM demonstrated diminished AM thiols ( P ≤ 0.05), increased AM mitochondrial ROS ( P ≤ 0.05), increased AM TGF β 1 ( P ≤ 0.05) with increased TGF β 1 signaling ( P ≤ 0.05), and impaired phagocytosis ( P ≤ 0.05). KO AM mitochondrial ROS was modulated by exogenous GSH ( P ≤ 0.05). Conversely, TGF β 1 was reduced ( P ≤ 0.05) and impaired phagocytosis was rescued ( P ≤ 0.05) by exogenous GSH in the KO AM. These results suggest that an altered neonatal AM phenotype may contribute to the initiation of lung inflammation/infection in the CF lung. Modulation of the AM in the neonatal CF lung may potentially alter progression of disease.

Background Chronic alcohol exposure alters the function of alveolar macrophages (AM), impairing immune defenses in both adult and neonatal lungs. Fatty acid ethyl esters (FAEEs) are biological markers of prenatal alcohol exposure in newborns. FAEEs contribute to alcohol-induced mitochondrial (MT) damage in multiple organs. We hypothesized that in utero ethanol exposure would increase FAEEs in the neonatal lung and that direct exposure of neonatal AM to FAEEs would contribute to MT injury and cellular dysfunction. Methods FAEEs were measured in neonatal guinea pig lungs after ± in utero ethanol exposure via gas chromatography/mass spectrometry. The NR8383 cell line and freshly isolated neonatal guinea pig AM were exposed to ethyl oleate (EO) in vitro. MT membrane potential, MT reactive oxygen species generation (mROS), phagocytosis, and apoptosis were evaluated after exposure to EO ± the MT-specific antioxidant mito-TEMPO (mitoT) or ± the pan-caspase inhibitor Z-VAD-FMK. Whole lung FAEEs were compared using the Mann–Whitney U-test. Cellular results were analyzed using 1-way analysis of variance, followed by the Student–Newman–Keuls Method for post hoc comparisons. Results In utero ethanol significantly increased ethyl linoleate and the combinations of ethyl oleate + linoleate + linolenate (OLL), and OLL + stearate in the neonatal lung. In vitro EO caused significant MT dysfunction in both NR8383 and primary neonatal AM, as indicated by increased mROS and loss of MT membrane potential. Impaired phagocytosis and apoptosis were significantly increased in both the cell line and primary AM after EO exposure. MitoT conferred significant but only partial protection against EO-induced MT injury, as did caspase inhibition with Z-VAD-FMK. Conclusions In utero ethanol exposure increased FAEEs in the neonatal guinea pig lung. Direct exposure to the FAEE EO significantly contributed to AM dysfunction, in part via oxidant injury to the MT and in part via secondary apoptosis.

The article describes the theory, characters and performance of the linear array of photodetectors includes CCD, PDA, CMOS and InGaAs, presents fiber grating sensor demodulation technique using linear InGaAs array and designs the demodulation system based on this technique. Furthermore, the system is used to measure the strain and temperature respectively, and prove the system have a good practicability. The demodulation system has a high resolution and measurement precision, changes the size of traditional Fiber Grating Sensors demodulation system essentially, and realizes basically the intelligence of the FBG sensors and lays a foundation for the industrialization of the FBG sensors.

Background: The effects of in utero alcohol exposure on the immune function of the newborn remain under investigation. Fetal ethanol (ETOH) exposure increases oxidative stress in the developing lung, in part due to decreased availability of the antioxidant glutathione (GSH). We have previously shown that in utero ETOH impairs alveolar macrophage phagocytosis and viability in the premature pup, while maintaining GSH availability with maternal supplementation of S-adenosyl-methionine (SAM) during ETOH ingestion improves macrophage function and viability. We hypothesized that dysfunction of the neonatal alveolar macrophage exposed to ETOH in utero would persist at term gestation. Methods: Using a guinea-pig model of fetal ETOH exposure, timed-pregnant guinea-pigs were pair-fed ETOH±the GSH precursor SAM and the diet continued until spontaneous delivery. Term alveolar macrophages were evaluated using fluorescent microscopy for phagocytosis and apoptosis after in vitro incubation with Staphalococcus aureus. Using an in vivo model of intranasal Staph. aureus inoculation, the in vivo function of the term alveolar macrophage was also investigated using confocal fluorescent analysis. Results: In utero ETOH exposure increased oxidant stress in the alveolar macrophage and decreased phagocytosis and viability in vitro and in vivo. Confocal analysis of phagocytosis in vivo demonstrated a marked impairment of internalization of the bacteria by the ETOH-exposed alveolar macrophage. The addition of SAM during maternal ETOH ingestion prevented loss of alveolar macrophage function and viability in vitro and in vivo. Conclusions: In utero ETOH exposure impairs alveolar macrophage function and viability in vitro and in vivo even at term gestation. The ETOH-induced changes in macrophage function and viability can be ablated with maternal SAM supplementation. Further investigations are required to identify the mechanisms of ETOH-induced derangement of phagocytosis in the neonatal alveolar macrophage and the clinical ramifications of altered immune function after in utero alcohol exposure for the newborn.

Noroviruses (NoVs) are the most commonly identified cause of outbreaks and sporadic cases of acute gastroenteritis. We evaluated and optimized NoV-specific TaqMan real-time reverse transcription (RT)-PCR assays for the rapid detection and typing of NoV strains belonging to genogroups GI and GII and adapted them to the LightCycler platform. We expanded the detection ability of the assays by developing an assay that detects the GIV NoV strain. The assays were validated with 92 clinical samples and 33 water samples from confirmed NoV outbreaks and suspected NoV contamination cases. The assays detected NoV RNA in all of the clinical specimens previously confirmed positive by conventional RT-PCR and sequencing. Additionally, the TaqMan assays successfully detected NoV RNA in water samples containing low viral concentrations and inhibitors of RT and/or PCR, whereas the conventional method with region B primers required dilution of the inhibitors. By means of serially diluted NoV T7 RNA transcripts, a potential detection limit of

Immature function of the alveolar macrophage increases the risk of pulmonary infections in premature newborns. In utero alcohol increases fetal systemic oxidative stress. Because the premature lung is deficient in glutathione (GSH), we hypothesized that chronic in utero alcohol (ethanol) exposure exacerbates the oxidative stress within the developing lung, thereby impairing alveolar macrophage function. Additionally, we evaluated the effects of in vivo and in vitro GSH availability on ethanol-exposed macrophage function. Using a guinea pig model of chronic in utero ethanol exposure, fetal epithelial lining fluid (ELF) and alveolar macrophage GSH were decreased with increased markers of oxidative stress. Ethanol-exposed macrophage exhibited impaired phagocytosis and increased apoptosis compared with gestational control. When the GSH precursor S-adenosyl-methionine (SAM) was added to the maternal drinking water containing ethanol, fetal ELF and macrophage GSH were maintained and ELF oxidative stress diminished. In vivo maternal SAM therapy maintained macrophage phagocytosis and decreased apoptosis. In vitro GSH supplements also improved phagocytosis and viability in both premature and ethanol-exposed macrophage. This suggested that in utero ethanol impaired premature macrophage function and viability via decreased GSH availability. Furthermore, GSH supplementation during and after ethanol exposure improved fetal macrophage function and viability. These results add a new dimension to the detrimental effects of fetal alcohol exposure on the developing alveolar macrophage, raising the possibility of GSH therapy to augment premature alveolar macrophage function.

Excessive consumption of alcohol (EtOH), the 3 leading preventable cause of death in the USA, has been shown to lead to increased incidence and severity of acute respiratory distress syndrome. The increased risk of respiratory infections in alcoholics is believed to be due to alterations in alveolar macrophage (AM) function. Previous studies have shown chronic EtOH ingestion leads to increased oxidant stress, increased TGFb production, increased fibronectin production, and decreased phagocytosis in AMs. Alternative (M2) activation of AMs has also been shown to lead to similar alterations. Classical ‘‘M1’’ by T helper 1 (TH1) cytokines leads to a proinflammatory response that is required for the respiratory burst necessary for phagocytosis. However, M2 is induced by TH2 cytokines leads to increased arginase production, increased arginase activity, and increased proline and polyamine production. These events promote fibroblast proliferation, collagen production and fibrosis within the lung. Our aim was to determine if chronic EtOH treatment leads to alterations in the expression of markers of M2 activation in AMs. To test this hypothesis, NR8383 cells, a rat-derived alveolar macrophage cell line, were treated with 0.08% EtOH, 25mM acetylaldehyde (AA), or IL-13, a know activator of M2 activation, 6 GSH or 6 IL-13 neutralizing antibody for 5 days. The cells were then analyzed for arginase activity and expression, active TGF-b production in cell culture media, and fibronectin production by 3T3 cells, a fibroblast cell line. In NR8383 cells, treatment with EtOH, AA, or IL-13 led to increased arginase activity, increased arginase expression, active TGF-b production, and secretion of factors that promoted fibronectin production in 3T3 cells. Supplementation with GSH or IL-13 neutralizing antibody during the 5 day treatment led to partial normalization of arginase activity, arginase expression, active TGF-b production, and activation of 3T3 cells in fibronectin production. In conclusion, several markers of M2 activation were greatly increased in response to EtOH, AA, and IL-13 treatment and GSH/ IL-13 neutralizing antibody treatment blocked these effects suggesting chronic EtOH treatment leads to M2 activation of AMs and antioxidant treatment can partially prevent that switch.

Background Maternal alcohol abuse remains a significant problem for our society and ˜ 35% of women consume alcohol during pregnancy. Alcohol-induced injury is augmented in females compared to males. Although in utero alcohol exposure is known to increase oxidative stress in the developing fetus, the effects of alcohol use on the gravid female have not been thoroughly explored. Previous studies from our laboratory have demonstrated that in utero ethanol (ETOH) exposure increased fetal oxidative stress in part via a decrease in the availability of the antioxidant glutathione (GSH). We hypothesize that alcohol used during pregnancy increases oxidative stress and alters cytokines in the gravid female. Objective To 1) evaluate the effects of ETOH consumption on maternal markers of oxidative stress and proinflammatory cytokines and 2) evaluate the effects of GSH supplementation during ETOH ingestion in the gravid female. Methods Using a guinea pig model of fetal ETOH exposure, timed-pregnant guinea pigs were randomly assigned on ˜ d32 (term d70) to ± ETOH in drinking water up to 4% (25% calories + 8 mg/100 mL saccharin) by d40 gestation. Where appropriate the GSH donors SAM or NAC were added to the water containing the ETOH. Cesarean section was performed on d55 of gestation and maternal blood obtained. Malonyldialdehyde (MDA) a marker of oxidative stress, and the proinflammatory cytokines TNF-α and IL-6 were measured with commercially available ELISAs with values normalized to plasma protein. Values are mean (pg/μg protein) ± SEM. Results MDA was significantly increased with ETOH consumption (control 0.0142 ± 0.001, ETOH 0.0285 ± 0.00329, p Conclusions ETOH consumption during pregnancy increases systemic oxidative stress in the female dam. The addition of GSH donors during ETOH ingestion protects the dam from ETOH-induced oxidant stress. We speculate that alcohol ingestion during pregnancy increases the risk of oxidant and proinflammatory mediated injury in the female. Funded by NIH RO1 AA013972-02 (to T.W.G.).

We present an experimental and theoretical study of the absorption of the IR He–Ne laser (3.39 µm) by Ch4. Shocktube measurements were made for mixture of CH4 with Ar, N2, and O2 in wide density and temperature ranges. Calculations were made by using the available spectroscopic data on CH4 absorption lines. Comparison between experiments and calculations show that the theoretical predictions are accurate for all densities up to the temperature of 1200 K. At 2000 K, the calculations fail, probably due to insufficient knowledge of hot-band lines. Furthermore, the present study shows that mixture of CH4 with Ar, O2, and N2 lead to absorptions which are similar (within experimental error), as is confirmed by the theoretical model.

Background Analysis of exhaled breath condensates (EBC) is a non-invasive technique to evaluate biomarkers such as antioxidants in the pediatric population, but limited data exists of its use in intubated patients, particularly newborns. Currently, tracheal aspirate (TA) serves as the gold standard collection modality in critically ill newborns, but this method remains invasive. We tested the hypothesis that glutathione status would positively correlate between EBC and TA collections in intubated newborns in the Newborn Intensive Care Unit (NICU). We also hypothesized that these measurements would be associated with alveolar macrophage (AM) glutathione status in the newborn lung. Methods Reduced glutathione (rGSH), glutathione disulfide (GSSG), and total GSH (rGSH + (2 X GSSG)) were measured in sequential EBC and TA samples from 26 intubated newborns via high performance liquid chromatography (HPLC). Additionally, AM glutathione was evaluated via immunofluorescence. Pearson’s correlation coefficient and associated 95% confidence intervals were used to quantify the associations between raw and urea-corrected concentrations in EBC and TA samples and AM staining. Statistical significance was defined as p ≤ 0.05 using two-tailed tests. The sample size was projected to allow for a correlation coefficient of 0.5, with 0.8 power and alpha of 0.05. Results EBC was obtainable from intubated newborns without adverse clinical events. EBC samples demonstrated moderate to strong positive correlations with TA samples in terms of rGSH, GSSG and total GSH. Positive correlations between the two sampling sites were observed in both raw and urea-corrected concentrations of rGSH, GSSG and total GSH. AM glutathione staining moderately correlated with GSSG and total GSH status in both the TA and EBC. Conclusions GSH status in EBC samples of intubated newborns significantly correlated with the GSH status of the TA sample and was reflective of cellular GSH status in this cohort of neonatal patients. Non-invasive EBC sampling of intubated newborns holds promise for monitoring antioxidant status such as GSH in the premature lung. Further studies are necessary to evaluate the potential relationships between EBC biomarkers in the intubated premature newborn and respiratory morbidities.