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The athletic abilities of the horse serve as a valuable model to understand the physiology and molecular mechanisms of adaptive responses to exercise. We analyzed differentially expressed genes in triceps brachii muscle tissues collected from Eonjena Taeyang and Jigusang Seryeok Thoroughbred horses and their co-expression networks in a large-scale RNA-sequence dataset comparing expression before and after exercise. High-quality horse transcriptome data were generated, with over 22 million 90-bp pair-end reads. By comparing the annotations, we found that MYH3, MPZ, and PDE8B genes in Eonjena Taeyang and PDE8B and KIF18A genes in Jigusang Seryeok were upregulated before exercise. Notably further, we observed that PPP1R27, NDUFA3, TNC, and ANK1 in Eonjena Taeyang and HIF1A, BDNF, ADRB2, OBSCN, and PER3 in Jigusang Seryeok have shown upregulation at the postexercise period. This investigation suggested that genes responsible for metabolism and oxidative phosphorylations associated with endurance and resistance exercise were highly expressed, whereas genes encoding structural proteins were generally suppressed. The expression profile of racehorses at pre- and postexercise will provide credible reference for further studies on biological effects such as responses to stress and adaption of other Thoroughbred horse, which might be useful for selective breeding for improvement of traits in commercial production.

Background Idiopathic pulmonary fibrosis (IPF) is a progressive and fatal disease with no effective treatment. The epithelial-mesenchymal transition (EMT) is a critical stage during the development of fibrosis. To assess the effect of sulforaphane (SFN) on the EMT and fibrosis using an in vitro transforming growth factor (TGF)-β1-induced model and an in vivo bleomycin (BLM)-induced model. Methods In vitro studies, cell viability, and cytotoxicity were measured using a Cell Counting Kit-8. The functional TGF-β1-induced EMT and fibrosis were assessed using western blotting and a quantitative real-time polymerase chain reaction. The lungs were analyzed histopathologically in vivo using hematoxylin and eosin and Masson’s trichrome staining. The BLM-induced fibrosis was characterized by western blotting and immunohistochemical analyses for fibronectin, TGF-β1, E-cadherin (E-cad), and α-smooth muscle actin (SMA) in lung tissues. Results SFN reversed mesenchymal-like changes induced by TGF-β1 and restored cells to their epithelial-like morphology. The results confirmed that the expression of the epithelial marker, E-cadherin, increased after SFN treatment, while expression of the mesenchymal markers, N-cadherin, vimentin, and α-SMA decreased in A549 cells after SFN treatment. In addition, SFN inhibited TGF-β1-induced mRNA expression of the EMT-related transcription factors, Slug, Snail, and Twist. The SFN treatment attenuated TGF-β1-induced expression of fibrosis-related proteins, such as fibronection, collagen I, collagen IV, and α-SMA in MRC-5 cells. Furthermore, SFN reduced the TGF-β1-induced phosphorylation of SMAD2/3 protein in A549 cells and MRC-5 cells. BLM induced fibrosis in mouse lungs that was also attenuated by SFN treatment, and SFN treatment decreased BLM-induced fibronectin expression, TGF-β1 expression, and the levels of collagen I in the lungs of mice. Conclusions SFN showed a significant anti-fibrotic effect in TGF-β-treated cell lines and BLM-induced fibrosis in mice. These findings showed that SFN has anti-fibrotic activity that may be considered in the treatment of IPF. Electronic supplementary material The online version of this article (10.1186/s40360-018-0204-7) contains supplementary material, which is available to authorized users.

There are sporadic reports in the literature in which radiologic liver and lung lesions found incidentally during follow-up metastatic surveillance were shown to be caused by toxocariasis.The objective of the work discussed in this report was to identify common clinical and histopathological features of toxocariasis resembling metastatic nodules in five patients with gastrointestinal cancer.We retrospectively analyzed clinical features of five gastrointestinal cancer patients with liver or lung nodules mimicking metastasis. Serologic tests for parasitic infestations and pathologic examinations were performed.All five patients were males and three patients had gastric cancer and two had colorectal cancer. All the cases of toxocariasis were confirmed serologically. On follow-up imaging, the lesions improved or resolved, suggestive of the phenomenon of visceral larva migrans. In two patients, liver biopsy was performed and showed eosinophilic abscess.Serologic tests and liver or lung biopsy should be performed aggressively to exclude toxocariasis when patients with underlying gastrointestinal cancer present with hepatic or pulmonary nodules associated with eosinophilia, particularly if the patients have a clinical history of raw animal liver ingestion. Curative surgical intervention should not be excluded just because of multiple nodules in the liver or the lungs.

To determine the efficacy and safety of belotecan in combination with cisplatin as first-line chemotherapy for extensive disease of small cell lung cancer (ED SCLC).Patients with chemotherapy-naïve ED SCLC were eligible if the following criteria were met: age ≥18 years; a measurable lesion; Eastern Cooperative Oncology Group Performance Status (PS) 0-2; and adequate organ function. Each cycle consisted of belotecan (0.5 mg/m(2)/day) on days 1-4 and cisplatin (60 mg/m(2)) intravenously on day 1. The cycle was repeated every 3 weeks until the completion of the 6th cycle, disease progression, or intolerable toxicity.Thirty-five patients (median age, 68 years) were enrolled: 32 males (91.4%); and PS = 0 (n = 3), PS = 1 (n = 18), and PS = 2 (n = 14). The median number of cycles delivered was 5 (range, 1-6). The relative dose intensity was 70.1% for belotecan and 83.0% for cisplatin. Of 30 evaluable patients, objective response rate was 71.4% (95% confidence interval [CI], 55.7-87.2) by the intent-to-treat principle. The median duration of follow-up was 14.3 months. The median progression-free survival was 5.7 months (95% CI, 3.9-7.5) and the median overall survival was 10.2 months (95% CI, 9.3-11.1). The frequently reported grade 3 or 4 toxicities included neutropenia in 24 patients (68.6%), thrombocytopenia in 10 (28.6%), and anemia in 7 (20.0%). There was no grade 3 or 4 non-hematologic toxicity except three patients (8.6%) with fatigue.Belotecan and cisplatin combination therapy showed significant efficacy in ED SCLC with improved non-hematologic toxicities.

Although the efficacy of topotecan as a second-line chemotherapy for small-cell lung cancer (SCLC) has been consistently demonstrated in phase II/III clinical trials, the choice of irinotecan as the first-line therapy prevented the use of evidence-based option. This pilot study was conducted to determine the activity and safety of topotecan in SCLC patients refractory to first-line therapy with irinotecan and platinum.Patients with primary refractory (no response, or progression during oror =90 days after last chemotherapy) SCLC after treatment with a combination of irinotecan and platinum, received topotecan 1.5 mg/m(2) per day as a 30-min infusion daily for 5 days, every 3 weeks.Of 17 eligible patients, ten patients were previously treated with irinotecan plus cisplatin and 7 were treated with irinotecan plus carboplatin. The median age was 68 years (range 44-75) and the median interval from the last chemotherapy was 50 days (range 21-89). A total of 33 chemotherapy cycles were delivered (median 2; range 1-5). All 17 patients discontinued therapy due to disease progression and 5 patients had progressive disease before second cycle. Toxic effects were mainly hematologic (gradeor =3 neutropenia in 65% of patients) and fatigue (grade 3 in 47%). In an intent-to-treat analysis, two (12%) patients had a confirmed partial response and two patients achieved stable disease. Median progression-free and overall survivals were 1.7 months (95% CI, 1.5-1.9) and 3.4 months (95% CI, 1.7-5.0), respectively.Topotecan monotherapy for patients with irinotecan-refractory SCLC does not appear highly active but the observation of some responses merits further study in patients with chemosensitive disease.

Introduction Automatic fire suppression systems use hydrofluorocarbons (HF) to extinguish fires chemically. At high temperatures, HF can release hydrofluoric acid (HFA), a toxic, potentially lethal gas. Case report A 52-year-old male visited our Pulmonary Division with dyspnea of 8-months duration. He had been working at a facility that manufactured fire extinguishers. Bronchoscopy was performed and a transbronchial lung biopsy was taken from the right lower lobe. After the patient was diagnosed with pulmonary alveolar proteinosis (PAP), whole-lung lavage was performed. In this case, fire extinguisher gas induced pulmonary alveolar proteinosis. This material should be used with care and investigated further. Discussion HFA is corrosive and penetrates organic materials, including body tissues. Depending on the mode of exposure, skin ulceration, pulmonary injury, or even systemic shock can result. This report describes PAP that developed after chronic, repeated exposure to fire extinguisher spray. Hydrofluoric acid can induce pulmonary disorders such as PAP.

Background Interleukin-8 (IL-8) is a potent chemo-attractant cytokine responsible for neutrophil infiltration in lungs with idiopathic pulmonary fibrosis (IPF). The IL-8 protein and mRNA expression are increased in the lung with IPF. We evaluated the effect of single nucleotide polymorphisms (SNPs) of the IL-8 gene on the risk of IPF. Methods One promoter (rs4073T>A) and two intronic SNPs (rs2227307T>G and rs2227306C>T) of the IL-8 genes were genotyped in 237 subjects with IPF and 456 normal controls. Logistic regression analysis was applied to evaluate the association of these SNPs with IPF. IL-8 in BAL fluids was measured using a quantitative sandwich enzyme immunoassay, and promoter activity was assessed using the luciferase reporter assay. Results The minor allele frequencies of rs4073T>A and rs2227307T>G were significantly lower in the 162 subjects with surgical biopsy-proven IPF and 75 subjects with clinical IPF compared with normal controls in the recessive model (OR = 0.46 and 0.48, p = 0.006 and 0.007, respectively). The IL-8 protein concentration in BAL fluids significantly increased in 24 subjects with IPF compared with 14 controls (p = 0.009). Nine IPF subjects homozygous for the rs4073 T>A common allele exhibited higher levels of the IL-8 protein compared with six subjects homozygous for the minor allele (p = 0.024). The luciferase activity of the rs4073T>A common allele was significantly higher than that of the rs4073T>A minor allele (p = 0.002). Conclusion The common allele of a promoter SNP, rs4073T>A, may increase susceptibility to the development of IPF via up-regulation of IL-8.