In this study, we investigated the chemical profile and effects of RW0117 (Artemisia argyi 65 .5 % ethanol extract) on gastric lesions in rats. We optimized and validated a method to obtain the chemical profile of RW0117. We then investigated the antioxidant and anti-inflammatory effects in vivo, and the protective effects on gastric lesions in vivo. The IC50 of 2,2-diphenyl-1-picrylhydrazyl free radical scavenging considering the antioxidant effects of RW0117 was 166.55 μg/mL, and the IC50 of nitric oxide scavenging considering the antiinflammatory effects was 41.16 μg/mL. Oral administration of RW0117 at lower concentrations (25, 50, 100 mg/ kg) had similar or greater effects than the daily intake conversion concentration (115mg/kg) of a health functional food (Avexol® ) in the acetic acid-induced ulcer and the ethanol-induced gastric injury rat models. In addition, oral administration of RW0117 increased the expression of prostaglandin E2 , which enhances the protective effect in the gastric mucosa in the ethanol-induced gastric injury rat model. These results suggest that RW0117 may have potential therapeutic uses in the protection of the gastric mucosa.

In this study, we investigated the chemical profile and effects of RW0117 (Artemisia argyi 65 .5 % ethanol extract) on gastric lesions in rats. We optimized and validated a method to obtain the chemical profile of RW0117. We then investigated the antioxidant and anti-inflammatory effects in vivo, and the protective effects on gastric lesions in vivo. The IC50 of 2,2-diphenyl-1-picrylhydrazyl free radical scavenging considering the antioxidant effects of RW0117 was 166.55 μg/mL, and the IC50 of nitric oxide scavenging considering the antiinflammatory effects was 41.16 μg/mL. Oral administration of RW0117 at lower concentrations (25, 50, 100 mg/ kg) had similar or greater effects than the daily intake conversion concentration (115mg/kg) of a health functional food (Avexol® ) in the acetic acid-induced ulcer and the ethanol-induced gastric injury rat models. In addition, oral administration of RW0117 increased the expression of prostaglandin E2 , which enhances the protective effect in the gastric mucosa in the ethanol-induced gastric injury rat model. These results suggest that RW0117 may have potential therapeutic uses in the protection of the gastric mucosa.

We hereby report a case on bronchogenic cyst which is initially non-infected, then becomes infected after bronchoscopic ultrasound (US)-guided transesophageal fine-needle aspiration (FNA). The non-infected bronchogenic cyst appears to be filled with relatively echogenic materials on US, and the aspirate is a whitish jelly-like fluid. Upon contrast-enhanced MRI of the infected bronchogenic cyst, a T1-weighted image shows low signal intensity and a T2-weighted image shows high signal intensity, with no enhancements of the cyst contents, but enhancements of the thickened cystic wall. The patient then undergo video-assisted thoracic surgery 14 days after the FNA. The cystic mass is known to be completely removed, and the aspirate is yellowish and purulent. To understand the image findings that pertain to the gross appearance of the cyst contents will help to diagnose bronchogenic cysts in the future.
Biopsy, Fine-Needle ; Bronchogenic Cyst* ; Humans ; Magnetic Resonance Imaging ; Thoracic Surgery, Video-Assisted ; Ultrasonography

No abstract available.
Carcinoma, Hepatocellular/*complications/*secondary/therapy ; Embolization, Therapeutic ; Fatal Outcome ; Hemothorax/diagnosis/*etiology/therapy ; Humans ; Liver Neoplasms/*complications/*pathology/therapy ; Lymph Nodes/*pathology ; Lymphatic Metastasis ; Male ; Mediastinum ; Middle Aged ; Paracentesis ; Rupture, Spontaneous ; Tomography, X-Ray Computed ; Treatment Outcome

PURPOSE: Estrogen receptor (ER) is the key therapeutic target in breast cancer. ERbeta has recently been identified to be distinct from ERalpha. In contrast to ERalpha, the functions of ERbeta in breast cancer are still unclear. We sought to determine whether the expression of ERbeta can be used as a predictive marker for endocrine therapy for patients with ERalpha-negative breast cancer. METHODS: Formalin-fixed, paraffin-embedded tumor specimens from 52 patients with ER-/PR+ invasive breast cancer were immunostained for their ERbeta expression. These patients were treated with adjuvant tamoxifen. The results were correlated with various clinicopathological variables and the follow-up data. The expressions of p53 and HER-2/neu were also analyzed and correlated with the ERbeta status. RESULTS: An ERbeta expression was observed in 53.8% (28/52) of the breast cancer samples. There was no correlation between the ERbeta expression and the other clinicopathologic factors (age, tumor size, histologic type, nodal status, histological grade, stage, therapeutic modality, progesterone receptor (PR) expression, p53 expression and HER-2/neu expression). Recurrence was present in 7.7% (2/26) of the patients whose tumors had an ERbeta expression, as compared to the presence of recurrence in 36.4% (8/22) of the patients whose tumors had no ERbeta expression (p<0.05). The patients with ERbeta negative-tumors revealed lower disease free survival rate than those with ERbeta positive-tumors (p<0.05). Of the 52 patients, 10 (19.2%) were p53 positive, and 11 (21.2%) were HER-2/neu positive. No significant correlations were observed between ERbeta and p53 or HER-2/neu. CONCLUSION: These results suggest that ERbeta might be a predictive marker of a response to endocrine therapy in patients with ER-/PR+ invasive breast cancer, although this needs to be confirmed by additional studies.
Breast ; Breast Neoplasms ; Disease-Free Survival ; Estrogen Receptor alpha ; Estrogen Receptor beta ; Estrogens ; Follow-Up Studies ; Humans ; Progesterone ; Receptors, Progesterone ; Recurrence ; Tamoxifen

PURPOSE: Dendritic cells (DCs) are the most potent antigen- presenting cells for initiating the T cell immune response in vivo. Recent studies have shown that active immunotherapy with tumor antigen pulsed DC tumor antigen specific cytotoxic T lymphocyte (CTL) response. The aim of this study was to establish clinically compatible procedures for generating human DCs and to determine if the CEA peptide- pulsed DCs can activate the CEA specific CTL responses in vitro. METHODS: DCs were generated from the peripheral blood monocytes (PBMCs) of HLA A2+ healthy donors using GM-CSF and IL-4. Phenotypic analysis was performed using flow cytometry with FITC- or PE-conjugated Abs against CD1a, CD14, CD80, HLA-DR, CD83 and CD86. The immature DCs were pulsed with a CEA peptide (HLA A2 epitope, [YLSGANLNL]) and the tumor lysates isolated from HLA A2+ CEA positive cell line, NCI-H498, and were incubated with the autologous PBMCs in order to generate an antigen specific CTLs in vitro. After three rounds of stimulation, the presence of a CEA-specific CTL response was determined using a CEA positive cell line as the specific targets with the standard 51Cr release assay, the ELISPOT assay, and the flow cytometry using CEA peptide-MHC tetramer. RESULTS: The DCs obtained after 6 days of culture expressed high levels of CD1a, HLA-DR, and CD80, which corresponded to the immature DC phenotype. The 51Cr- release assay showed that DCs pulsed with the CEA peptide or the lysates of the CEA-positive NCI-H498 cell line could stimulate the CEA-specific CTL responses. The CTL response to DCs pulsed with the CEA peptide was also generated using the DCs pulsed with the CEA peptide. In the ELISPOT assay, the number of CEA peptide-specific, INF-gamma-secreting spots were increased in the CTLs generated by DCs pulsed with the CEA pepide and the tumor lysates. In the peptide-MHC tetramer assay, the CD8+ T cells with the receptors specific to CEA-peptide were increased by stimulation with the DCs pulsed with the CEA peptide and the tumor lysates. CONCLUSION: These findings show that the CEA peptide pulsed DCs can generate CEA specific CTL responses and antigen bearing DCs can be used as the target cells for a cytotoxicity assay. This study provides the foundations for DC-based cancer immunotherapy for CEA expressing solid tumors.
Carcinoembryonic Antigen* ; Cell Line ; Dendritic Cells* ; Enzyme-Linked Immunospot Assay ; Flow Cytometry ; Foundations ; Granulocyte-Macrophage Colony-Stimulating Factor ; HLA-DR Antigens ; Humans ; Immunotherapy ; Immunotherapy, Active ; Interleukin-4 ; Lymphocytes ; Monocytes ; Phenotype ; T-Lymphocytes ; T-Lymphocytes, Cytotoxic* ; Tissue Donors