Loranthus tanakae Franch. and Sav. Attenuates Respiratory Inflammation Caused by Asian Sand Dust.

Asian sand dust (ASD), generally produced in East Asia, including China, Japan, and Korea, directly leads to the development of pulmonary disease and exacerbates underlying pulmonary diseases. Loranthus tanakae Franch. and Sav. is a traditional herbal medicine applied to improve various inflammatory conditions. Here, we evaluated the curative properties of L. tanakae ethanol extract (LTE) against pulmonary inflammation caused by ASD. Additionally, to investigate the mechanism of action of LTE, we performed network pharmacological analysis. ASD was administrated on day 1, 3, and 5 by intranasal instillation, and LTE was orally administered for 6 days. Administration of LTE significantly decreased inflammatory cytokines and the number of inflammatory cells in bronchoalveolar lavage fluid, which was accompanied by a decrease in inflammatory cell accumulation in pulmonary tissue. Administration of LTE decreased the expression of cyclooxygenase2 and matrix metalloproteinase-9 in mice exposed to ASD with the decline in p65 phosphorylation. Additionally, administration of LTE significantly elevated hemeoxygenase (HO)-1 expression in the pulmonary tissue of mice exposed to ASD. These results were consistent with the data of network pharmacological analysis. This experiment showed that LTE attenuated pulmonary inflammation caused by ASD via inhibition of NF-κB and elevation of HO-1. Therefore, LTE may have potential as a therapeutic agent to treat pulmonary inflammation caused by ASD.

The effects of Pycnogenol, a pine bark extract on pulmonary inflammation by Asian sand dust in mice.

Asian sand dust (ASD), also called China dust or yellow dust, mainly occurs in East Asia during spring and autumn. Because ASD enters the body mainly through the respiratory system, it can cause respiratory disorders or worsen underlying diseases. Because of this, it has become an important health concern that threatens the well-being of humans and animals. In this study, we investigated the effects of 15 and 30 mg/kg of Pycnogenol (PYC15 and 30 groups), a pine bark extract, on ASD-induced pulmonary inflammation in mice. We evaluated the inflammatory cell counts, inflammatory cytokines, and matrix-metalloproteinase (MMP)-9 expression in animal models. PYC administration significantly decreased inflammatory cell infiltration into lung tissue; this was accompanied by a reduction in the levels of proinflammatory mediators including interleukin (IL)-1ß (P < 0.01), IL-6 (P < 0.01) and tumour necrosis factor-α (P < 0.01) in bronchoalveolar lavage fluids of ASD-exposed mice (ASD group). Histological analysis revealed that PYC suppressed ASD-induced pulmonary inflammation. Moreover, PYC suppressed the levels of matrix-metalloproteinase (MMP)-9 in the lung tissue of ASD-exposed mice, indicating that PYC reduced ASD-induced pulmonary inflammation by suppressing MMP-9. Together, these results indicate that PYC as the potential to treat ASD-driven pulmonary inflammation.

ABSORBED DOSE AND IMAGE QUALITY ACCORDING TO THE SCAN MODE AND SHIELD POSITION IN PEDIATRIC BRAIN COMPUTED TOMOGRAPHY SCANS.

In this study, computed tomography dose index (CTDIvol), dose-length product (DLP), organ dose and signal-to-noise ratio (SNR) were measured in pediatric brain helical and volumetric CT scans using a pediatric phantom (equivalent to a 10-year-old) and optically stimulated luminescence dosemeters (OSLD) as the scan protocol used in Hospital A. Volumetric scans showed lower CTDIvol, DLP and organ dose than helical scans, and the SNR showed similar results. The organ doses were lower in the phantoms protected with front, rear or front and rear shielding than in those without shielding. However, no statistically significant differences were found among the different shield locations. In pediatric brain CT scans, to reduce exposure dose and patient discomfort while maintaining image quality, a volumetric scan rather than a helical scan was preferred, and a good shielding effect was observed with front or rear shielding.

Measurement of renal cortical thickness using ultrasound in normal dogs: a reference range study considering bodyweight and body condition score.

The renal cortical thickness (RCT) reflects the pathological condition of the kidney, and measuring this parameter can help diagnose renal fibrosis in dogs. The normal reference range of RCT in dogs is broad (3-8 mm) because of the extreme diversity in body size. Therefore, this retrospective, reference interval, and observational design study aimed to establish a normal reference range for RCT in dogs measured using ultrasound by considering bodyweight (BW), body surface area (BSA), body condition score (BCS), and abdominal aorta (Ao) diameter. A total of 60 dogs met the inclusion criteria, and abdominal ultrasound images and medical records of these dogs were analyzed. RCT was measured at 1-3 points where the renal capsule and broad base of the medullary pyramid were clearly observed. Ao diameter was measured caudal to the branch of the left renal artery in the mid-sagittal view. The RCT showed positive correlations with BW and BSA and a negative correlation with BCS, which can be described as follows: RCT (mm) = 0.131 × BW - 0.166 × BCS + 3.580. The RCT:Ao ratio was 0.70 ± 0.09 (mean ± standard deviation). No significant differences were found in the RCT:Ao ratio depending on BW or BCS. In conclusion, the RCT:Ao ratio and relative RCT considering both BW and BCS are potentially useful for evaluating the normality of the renal cortex on ultrasound examination in dogs with various physiques.

The Involvement of PDE4 in the Protective Effects of Melatonin on Cigarette-Smoke-Induced Chronic Obstructive Pulmonary Disease.

Chronic obstructive pulmonary disease (COPD) is a significant disease threatening human health. Currently, roflumilast, a phosphodiesterase (PDE)4 inhibitor, is recommended as a therapeutic agent for COPD. In this study, we investigated the therapeutic effects of melatonin against COPD, focusing on determining whether it is a PDE4 inhibitor via in vivo and in vitro experiment using cigarette smoke (CS) and cigarette smoke condensate (CSC), respectively. In the in vivo experiments, melatonin treatment reduced inflammatory responses, including inflammatory cell counts. Melatonin treatment also suppressed the CS-exposure-induced upregulation of cytokine and matrix metalloproteinase (MMP)-9, reduced the PDE4B expression, and elevated cAMP levels. In addition, these effects were synergistic, as melatonin and roflumilast cotreatment eventually ameliorated the CS-exposure-induced worsening of lung function. In the CSC-stimulated NCI-H292 cells, melatonin inhibited elevation in the levels of inflammatory cytokines, MMP-9, and PDE4, and elevated cAMP levels. Furthermore, melatonin and roflumilast cotreatment was more effective on inflammatory responses than only melatonin or roflumilast treatment. Our results indicate that melatonin relieves inflammatory response and loss of lung function in COPD, which is associated with decreased PDE4 expression. Therefore, we suggest that melatonin is a putative candidate for the treatment of COPD.

Melatonin Alleviates Silica Nanoparticle-Induced Lung Inflammation via Thioredoxin-Interacting Protein Downregulation.

Silica dioxide nanoparticles (SiONPs) have been increasingly used in various industries; however, this has raised concerns regarding their potential toxicity. SiONPs are also a major component in the Asian sand dust that causes pulmonary diseases among the general public. Melatonin exerts some inhibitory effects against lung inflammation. In this study, we explored the therapeutic properties of melatonin against lung inflammation using an SiONPs-induced lung inflammation murine model and SiONPs-stimulated H292 cells, human airway epithelial cell line, by focusing on the involvement of thioredoxin-interacting protein (TXNIP) in the modulation of the MAPKs/AP-1 axis. We induced an inflammatory response by exposing mouse lungs and the H292 cells to SiONPs and confirmed the anti-inflammatory effect of melatonin. Melatonin inhibited the expression of various inflammatory mediators, including TNF-α, IL-6, and IL-1ß, in SiONPs-exposed mice and SiONPs-stimulated H292 cells; this inhibition contributed to a decline in inflammatory cell accumulation in the lung tissues. Furthermore, melatonin treatment decreased the expression of MAPKs and AP-1 by downregulating TXNIP, eventually decreasing the production of SiONPs-induced inflammatory mediators. Overall, these data suggest that melatonin reduces SiONPs-induced lung inflammation by downregulating the TXNIP/MAPKs/AP-1 signalling pathway, thereby supporting the use of melatonin as an effective approach to control SiONPs-induced lung inflammation.

Case Report: Multimodality Imaging of Infectious Sacroiliitis and Retroperitoneal Abscess Causing Hindlimb Ataxia in a Young Dog.

A 3-month-old intact male Labrador Retriever was presented for falling trauma and hindlimb ataxia. Radiography indicated radiolucent left sacroiliac joint with irregular margin. Computed tomography revealed thickened sublumbar muscles and hypoattenuated sacroiliac joint while magnetic resonance imaging demonstrated abscess at retroperitoneum and gluteal muscle. Ultrasonography showed lytic left sacroiliac joint with retroperitoneal fluid, and fine needle aspiration resulted Staphylococcus aureus. Hindlimb ataxia was attributed to infectious sacroiliitis and its secondary retroperitoneal abscess. As far as the authors' knowledge, this is the first report of multimodality imaging of infectious sacroiliitis with retroperitoneal abscess caused by S. aureus in a dog.

Comparison of dental radiography and computed tomography: measurement of dentoalveolar structures in healthy, small-sized dogs and cats.

BACKGROUND: Dental diseases are common in dogs and cats, and accurate measurements of dentoalveolar structure are important for planning of treatment. The information that the comparison computed tomography (CT) with dental radiography (DTR) is not yet reported in veterinary medicine. OBJECTIVES: The purpose of this study was to compare the DTR with CT of dentoalveolar structures in healthy dogs and cats, and to evaluate the CT images of 2 different slice thicknesses (0.5 and 1.0 mm). METHODS: We included 6 dogs (2 Maltese and 1 Spitz, Beagle, Pomeranian, mixed, 1 to 8 years, 4 castrated males, and 2 spayed female) and 6 cats (6 domestic short hair,8 months to 3 years, 4 castrated male and 2 spayed female) in this study. We measured the pulp cavity to tooth width ratio (P/T ratio) and periodontal space of maxillary and mandibular canine teeth, maxillary fourth premolar, mandibular first molar, maxillary third premolar and mandibular fourth premolar. RESULTS: P/T ratio and periodontal space in the overall dentition of both dogs and cats were smaller in DTR compared to CT. In addition, CT images at 1.0 mm slice thickness was generally measured to be greater than the images at 0.5 mm slice thickness. CONCLUSIONS: The results indicate that CT with thin slice thickness provides more accurate information on the dentoalveolar structures. Additional DTR, therefore, may not be required for evaluating dental structure in small-sized dogs and cats.

Silibinin Attenuates Silica Dioxide Nanoparticles-Induced Inflammation by Suppressing TXNIP/MAPKs/AP-1 Signaling.

Silica dioxide nanoparticles (SiONPs) have been applied to several fields, such as drug delivery and gene therapy. However, SiONPs are a constituent of fine dust and can induce excessive inflammatory responses in the lungs via the airways. Silibinin, a major component of silymarin, has been known for its anti-oxidant and anti-inflammatory effects. In the present study, we explored the protective effects of silibinin against SiONPs-induced airway inflammation and explored its underlying mechanism of action, focusing on thioredoxin-interacting protein (TXNIP)/mitogen-activated protein kinases (MAPKs) in vitro and in vivo. In SiONPs-stimulated NCI-H292 airway epithelial cells, silibinin treatment effectively suppressed the elevation of the mRNA expression of tumor necrosis factor-α (TNF-α), interleukin (IL)-6, and IL-1ß, which was accompanied by the reduction in the expression of TXNIP, MAPKs, and activator protein-1 (AP-1). In SiONPs-treated mice, silibinin administration inhibited the increase in inflammatory cell counts and proinflammatory mediators, and it alleviated airway inflammation by SiONPs exposure. In addition, silibinin administration effectively suppressed the elevation of TXNIP/MAPKs/AP-1 signaling by SiONPs exposure. Taken together, silibinin effectively inhibited SiONPs-induced inflammatory responses, and this effect was closely related to the inhibition of TXNIP/MAPK/AP-1 signaling. These results suggested that silibinin might be useful for reducing pulmonary inflammation induced by SiONPs.

So-Cheong-Ryoung-Tang Attenuates Pulmonary Inflammation Induced by Cigarette Smoke in Bronchial Epithelial Cells and Experimental Mice.

So-Cheong-Ryoung-Tang is a traditionally used herbal formula for the treatment of pulmonary diseases in China, Korea, and Japan. We investigated the protective effects of So-Cheong-Ryong-Tang water extract (SCWE) in cigarette smoke concentrate (CSC) stimulated human airway epithelial cell line NCI-H292 and mice exposed cigarette smoke (CS) and lipopolysaccharide (LPS). In the CSC-stimulated NCI-H292 cells, SCWE inhibited proinflammatory cytokines in a concentration-dependent manner, as evidenced by a reduction in their mRNA levels. Also, SCWE significant reduced inducible nitric oxide synthase (iNOS) expression and nuclear factor kappa B (NF-κB) phosphorylation in CSC-stimulated cells. The mice were exposed to CS for 1 h per day (a total of eight cigarettes per day) for 7 days and received LPS intranasally on day 5. The mice were administered a dose of SCWE (100 and 200 mg/kg) 1 h before CS exposure. In in vivo, SCWE decreased the inflammatory cell count and reduced the expression of the proinflammatory cytokines in the broncho-alveolar lavage fluid (BALF) compared with CS and LPS exposed mice. SCWE attenuated inflammatory cell infiltration in airway induced by CS and LPS exposure, and this decrease was accompanied by a reduction in the expression levels of iNOS and MMP-9 in lung tissue. The extract also inhibited the phosphorylation of inhibitor of kappa B alpha (IκBα) and NF-κB induced by CS and LPS exposure in lung tissue. These results suggest that SCWE may effectively inhibit airway inflammatory responses induced by CS and LPS exposure via the NF-κB pathway. Therefore, SCWE may be a potential treatment for airway inflammatory diseases, such as chronic obstructive pulmonary disease (COPD).

Galgeun-tang Attenuates Cigarette Smoke and Lipopolysaccharide Induced Pulmonary Inflammation via IκBα/NF-κB Signaling.

Galgeun-tang water extract (GGWE) is used to treat various diseases such as the common cold, eczema and asthma in China and Korea. In this study, we investigated the anti-inflammatory effect of GGWE using a cigarette smoke (CS)- and lipopolysaccharide (LPS)-induced induced pulmonary inflammation mouse model. The mice were exposed to CS for a total of seven days (eight cigarettes per day for 1 h) and LPS was administered intranasally to mice on day 4. GGWE was administered by oral gavage at doses of 50 mg/kg or 100 mg/kg 1 h before exposure to CS. GGWE decreased inflammatory cell counts, and expression of inflammatory cytokines such as interleukin (IL)-6 and tumor necrosis factor alpha (TNF-α) in bronchoalveolar lavage fluid (BALF) from mice exposed to CS and LPS. GGWE reduced the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), as well as the phosphorylation of inhibitor of kappa-B subunit alpha (IκBα) and nuclear factor kappa-B (NF-κB) in CS- and LPS-exposed mice. Histological examinations revealed that GGWE suppressed inflammatory cell infiltration into lung tissue compared to untreated CS- and LPS-exposed mice. In conclusion, GGWE effectively suppressed CS- and LPS-induced pulmonary inflammation. Our results indicate that GGWE may be used as a protective drug to control pulmonary inflammation diseases such as chronic obstructive pulmonary disease.

Lobeglitazone Attenuates Airway Inflammation and Mucus Hypersecretion in a Murine Model of Ovalbumin-Induced Asthma.

Lobeglitazone (LB) is a novel agonist of peroxisome proliferator-activated receptor (PPAR)-α and γ that was developed as a drug to treat diabetes mellitus. We explored the ameliorative effects of LB on allergic asthma using a murine model of ovalbumin (OVA)-induced asthma. To boost the immune response of animals, OVA sensitization was performed on days 0 and 14. LB (250 or 500 µg/kg) was administered by oral gavage on days 18 to 23, and the OVA challenge was performed using an ultrasonic nebulizer on days 21 to 23. Plethysmography showed airway hyperresponsiveness (AHR) on day 24. LB treatment effectively decreased inflammatory cell recruitment, T-helper type 2 cytokines in the bronchoalveolar lavage fluid, and immunoglobulin (Ig) E in the serum of the animals with OVA-induced asthma, which was accompanied by a marked reduction in AHR. It also decreased airway inflammation, mucus hypersecretion, phosphorylation of nuclear transcription factor-kappa-B (NF-κB), and expression of activating protein (AP)-1 and mucin 5AC (MUC5AC). Overall, LB effectively attenuated the pathophysiological changes of asthma and its effects appear related to a reduction in the phosphorylation of NF-κB and the expression of AP-1. Thus, our results suggest that LB has a potential to treat allergic asthma.

Bronchoalveolar lavage affects computed tomographic and radiographic characteristics of the lungs in healthy dogs.

Bronchoalveolar lavage is a common diagnostic test for dogs with suspected pulmonary disease, however there is no published information on whether this procedure could affect the imaging characteristics of the lungs. Aims of this prospective experimental study were to describe computed tomography (CT) and radiographic features of the lungs after bronchoalveolar lavage in a sample of healthy dogs. Thoracic CT and radiographic images of eight healthy Beagles were acquired at the following time points: before bronchoalveolar lavage, immediately following bronchoalveolar lavage, and at 2, 4, 8, 12, and 24 h following bronchoalveolar lavage. Lung consolidation or interstitial patterns were seen in CT and radiographic images immediately after the procedure. Radiographic lung patterns resolved within 2 h and CT patterns resolved within 24 h. Resolution of the CT pulmonary patterns in the ventral areas of the lungs was delayed compared to the dorsal areas. Mean CT imaging scores differed over time (P < 0.001), while mean radiographic imaging scores did not differ over time. This study suggests that thoracic radiography and CT imaging assessments should precede bronchoalveolar lavage procedures if possible, or be performed at least 24 h afterward.

Genipin inhibits allergic responses in ovalbumin-induced asthmatic mice.

Genipin is a natural compound isolated from the fruit of Gardenia jasminoides with various pharmacological effects. In this study, we investigated whether genipin effectively alleviates allergic responses in a murine model of ovalbumin (OVA)-induced asthma. The mice were administered an intraperitoneal injection of OVA on day 0 and 14 to boost the immune response; genipin was then administered from day 18 to 23 by oral gavage. On days 21 to 23, mice were OVA-challenged using am ultrasonic nebulizer, and airway hyperresponsiveness (AHR) was determined on day 24 by plethysmography. Genipin significantly reduced the inflammatory cell count in bronchoalveolar lavage fluids (BALF) and AHR, which were accompanied by lower interleukin-5 (IL-5), IL-13 and OVA-specific immunoglobulin (Ig) E levels in the BALF or serum from OVA-induced asthmatic mice. In histology, genipin significantly decreased airway inflammation and mucus hypersecretion in OVA-induced asthmatic mice. Additionally, genipin inhibited OVA-induced increases in the expression of inducible nitric oxide synthase and cyclooxygenase-2 proteins. Further, genipin reduced the activity and protein levels of matrix metalloproteinase-9 in lung tissue from OVA induced asthmatic mice. Overall, genipin effectively alleviated the asthmatic inflammatory response in an OVA-induced asthmatic model. Therefore, our results suggest that genipin has therapeutic potential for treating asthma.

4-Hydroxycinnamic acid protects mice from cigarette smoke-induced pulmonary inflammation via MAPK pathways.

Cigarette smoke (CS) is the main etiological cause of chronic obstructive pulmonary disease, the prevalence of which has continuously increased in recent years. 4-Hydroxycinnamic acid (HA) is a plant phenolic acid that has anti-inflammatory activities. In this study, we explored the therapeutic effects of HA on airway inflammation caused by CS and lipopolysaccharide (LPS) in mice. The animals received 1 h of CS exposure for 7 days and intranasal instillation of LPS on day 4. HA (10 and 20 mg/kg) was administered to animals via oral gavage 1 h before CS exposure. HA treatment significantly decreased the accumulation of inflammatory cells and production of cytokines, including tumor necrosis factor-α, interleukin (IL)-6, and IL-1ß, caused by CS and LPS exposure. After histological examination, we observed that HA treatment significantly reduced the infiltration of inflammatory cells into lung tissue caused by CS and LPS exposure. Furthermore, HA-treated groups showed significantly decreased phosphorylation of extracellular signal-regulated kinase, c-Jun N-terminal kinase, p38, and nuclear factor-κB, and activity of cytochrome c oxidase subunit-2 caused by CS and LPS. In conclusion, HA effectively suppresses the airway inflammatory response induced by CS and LPS exposure, and is closely associated with the downregulation of mitogen-activated protein kinases signaling.

Pine bark extract (Pycnogenol®) suppresses cigarette smoke-induced fibrotic response via transforming growth factor-ß1/Smad family member 2/3 signaling.

Chronic obstructive pulmonary diseases (COPD) is an important disease featured as intense inflammation, protease imbalance, and air flow limitation and mainly induced by cigarette smoke (CS). In present study, we explored the effects of Pycnogenol® (PYC, pine bark extract) on pulmonary fibrosis caused by CS+lipopolysaccharide (LPS) exposure. Mice were treated with LPS intranasally on day 12 and 26, followed by CS exposure for 1 h/day (8 cigarettes per day) for 4 weeks. One hour before CS exposure, 10 and 20 mg/kg of PYC were administered by oral gavage for 4 weeks. PYC effectively reduced the number of inflammatory cells and proinflammatory mediators caused by CS+LPS exposure in bronchoalveolar lavage fluid. PYC inhibited the collagen deposition on lung tissue caused by CS+LPS exposure, as evidenced by Masson's trichrome stain. Furthermore, transforming growth factor-ß1 (TGF-ß1) expression and Smad family member 2/3 (Smad 2/3) phosphorylation were effectively suppressed by PYC treatment. PYC markedly reduced the collagen deposition caused by CS+LPS exposure, which was closely involved in TGF-ß1/Smad 2/3 signaling, which is associated with pulmonary fibrotic change. These findings suggest that treatment with PYC could be a therapeutic strategy for controlling COPD progression.

Silibinin inhibits the fibrotic responses induced by cigarette smoke via suppression of TGF-ß1/Smad 2/3 signaling.

Cigarette smoke (CS) is generally accepted as a major contributor to chronic obstructive pulmonary disease (COPD) which is characterized by chronic inflammation, fibrotic response, and airway obstruction. In this study, we investigated the preventive effects of silibinin, an active constitute of silymarin on CS and lipopolysaccharide (LPS) exposure-induced fibrotic response. Mice were exposed to CS for 1 h per day (8 cigarettes per day) for 4 weeks. On day 12 and 26, mice were treated with LPS intranasally. Silibinin (10 or 20 mg/kg) was administered orally 1 h before CS exposure. Silibinin markedly decreased the inflammatory cell count in the bronchoalveolar lavage fluid, and reduced levels of proinflammatory mediators. Silibinin suppressed CS + LPS-induced collagen deposition in lung tissue, as evidenced via immunohistochemistry and Masson's trichrome stain. Additionally, silibinin effectively inhibited CS + LPS-mediated expression of transforming growth factor-ß1 (TGF-ß1) and Smad 2/3 phosphorylation. Taken together, our data indicate that silibinin effectively inhibits the fibrotic response induced by CS + LPS exposure, possibly via suppression of TGF-ß1/Smad 2/3 signaling, which results in reduced collagen deposition. These findings suggest that silibinin has therapeutic potential for the treatment of COPD.

Protective effect of HwangRyunHaeDok-Tang water extract against chronic obstructive pulmonary disease induced by cigarette smoke and lipopolysaccharide in a mouse model.

ETHNOPHARMACOLOGICAL RELEVANCE: Hwangryunhaedok-tang is an oriental herbal formula treated to cure inflammation and gastric disorders in China, Japan, and Korea. We explored the protective effects of Hwangryunhaedok-tang water extract (HRWE) against airway pathophysiological changes caused by cigarette smoke (CS) and lipopolysaccharide (LPS) in a mouse. MATERIALS AND METHODS: We performed quantitative analyses of five marker components, namely geniposide, baicalin, coptisine, plamatine, and berberine, using high-performance liquid chromatography. Animals were received CS exposure (1h per day) for 7 days. LPS was administered intranasally on day 4. Mice were received HRWE at dose of 100 or 200mg/kg for 1h before CS exposure. RESULTS: Treatment with HRWE significantly suppressed the increased inflammatory cell count induced by CS and LPS exposure. In addition, reduction in IL-6, TNF-α and IL-1ß in broncho-alveolar lavage fluid (BALF) was observed after HRWE treatment. HRWE not only decreased inflammatory cell infiltration in lung, but also decreased the expression of iNOS, NF-κB and matrix metallopeptidase (MMP)-9 in lung tissues. CONCLUSION: This study showed that HRWE can attenuate respiratory inflammation caused by CS and LPS exposure. Therefore, HRWE has potential for treating airway inflammatory disease.

Time-dependent low-field MRI characteristics of canine blood: an in vitro study.

This study was conducted to assess time-sensitive magnetic resonance (MR) changes in canine blood using low-field MR. Arterial and venous blood samples were collected from eight healthy beagle dogs. Samples were placed in 5-mL tubes and imaged within 3 hours of collection at 1 day intervals from day 1 to day 30. The following sequences were used: T1-weighted (T1W), T2-weighted (T2W), fluid-attenuated inversion recovery (FLAIR), short tau inversion recovery (STIR), and T2-star gradient-echo (T2(*)-GRE). Visual comparison of the images revealed that four relatively homogenous blood clots and twelve heterogeneous blood clots developed. The margination of the clot and plasma changed significantly on day 2 and day 13. On day 2, heterogeneous blood clots were differentiated into 2 to 3 signal layers in the T2W, T1W, and especially the STIR images. Hypointense signal layers were also detected in the blood clots in STIR images, which have T2 hypo, FLAIR hypo, and T1 hyper intense signals. In all images, these signal layers remained relatively unchanged until day 13. Overall, the results suggest that hematomas are complex on low-field MRI. Accordingly, it may not be feasible to accurately characterize hemorrhages and predict clot age based on low-field MRI.

Copper oxide nanoparticle induces inflammatory response and mucus production via MAPK signaling in human bronchial epithelial cells.

Copper nanoparticles (CuONPs) can pose risks to industrial workers. With increase of its applications especially in electronic fields, it is necessary to assess the toxicity of CuONPs, including pulmonary toxicity. In this study, we investigated the effect of CuONPs on human epithelial cell line H292. CuONPs treatment caused a significant increase in IL-6 and IL-8 mRNA expression and protein levels in H292 cells in a concentration-dependent manner. The mRNA expression and protein levels of MUC5AC were consistent with those of proinflammatory mediators. Additionally, CuONPs treatment increased phosphorylation of mitogen-activated protein kinases (MAPKs), Erk, JNK, and p-38 compared to that of control in a concentration-dependent manner. However, co-treatment with CuONPs and each MAPK inhibitor significantly decreased the phosphorylation of each MAPK, resulting in decreased mRNA expression and protein levels of proinflammatory mediators and MUC5AC compared to that in H292 cells only treated with CuONPs. In summary, CuONPs-induced inflammatory mediators and MUC5AC associated with MAPKs phosphorylation. Our results will provide useful information on CuONPs-induced pulmonary toxicity.