Case report: Two rare new cases of diaphragmatic bronchogenic cysts.

The bronchogenic cyst (BC) is a type of congenital anomaly that is most usually found in the mediastinum and lung, and rarely in the diaphragm. We report two cases of bronchogenic cysts originating from the left diaphragm. Case 1 involved a 50-year-old man who underwent computed tomography (CT) of the adrenal glands for hypertension, showing left adrenal changes. An adrenal CT at our hospital showed a space-occupying lesion above the left diaphragm. We performed a left-sided thoracotomy in the seventh intercostal space and found that the mass was entirely located in the diaphragm. Case 2 was a 58-year-old woman who underwent chest CT under a standard health check-up, and a subpleural lesion of approximately 4 cm was found in the posterior basal segment of the left inferior lung lobe. During thoracoscopic surgery, the mass was found to originate from the surface of the diaphragm, having no correlation with the lung tissue. The two cases of diaphragmatic bronchogenic cysts were confirmed by surgical pathology. Ectopic bronchogenic cysts arising from the diaphragm are very uncommon, and diaphragmatic bronchogenic cysts typically occur on the left side, in women, and in the angle between the vertebral column and the diaphragm. As far as we know, there are no relevant reports of intradiaphragmatic BCs similar to case 1, which was entirely located within the diaphragm. Most diaphragmatic BCs are located on the surface of the diaphragm and project toward the thoracic or abdominal cavities. Moreover, bilocular diaphragmatic bronchogenic cysts, similar to case 2, have not yet been reported.

Long noncoding RNA NSCLCAT1 increases non-small cell lung cancer cell invasion and migration through the Hippo signaling pathway by interacting with CDH1.

Metastatic growth is the leading cause of cancer-related death in non-small cell lung cancer (NSCLC). Metastasis is believed to be initiated by an increase in cell motility mediated by the loss of cell-cell adhesion because of the suppression of E-cadherin [encoded by cadherin 1 ( CDH1)]. However, very little is known about the molecular mechanism of CDH1 regulation. Therefore, we hypothesized that non-small cell lung cancer-associated transcript-1 (NSCLCAT1) suppresses functional CDH1 and mediates the Hippo signaling pathway, resulting in increased cell migration and invasion, and reduced apoptosis. Initially, microarray profiling and target prediction programs were employed to identify whether NSCLCAT1 targets CDH1. Next, quantitative PCR was used to determine the expression pattern of NSCLCAT1 in 114 specimens. The biologic functions of NSCLCAT1 in NSCLC were assessed through the up-regulation and down-regulation of the levels of endogenous NSCLCAT1 with the use of NSCLCAT1 vector or small interfering RNA against NSCLCAT1 in NSCLC cells. Furthermore, the Hippo signaling pathway in NSCLC cells was blocked by applying the verteporfin treatment to have a better understanding on the pivotal role of the Hippo signaling pathway in NSCLC. Microarray expression profiles of long noncoding RNAs, GSE19804 and GSE27262), revealed that NSCLCAT1 was up-regulated in NSCLC. Among patients with NSCLC, we determined that the NSCLCAT1 was robustly induced, whereas CDH1 was suppressed. The luciferase activity determination identified CDH1 as a NSCLCAT1 target. NSCLCAT1 was found to increase cell viability, migration, and invasion and to reduce apoptosis in NSCLC cells. The results from the quantitative PCR and Western blot analysis revealed that NSCLCAT1 modulated the Hippo signaling pathway. Furthermore, the inhibition of the Hippo signaling pathway by verteporfin treatment led to the loss of the effect of NSCLCAT1 on NSCLC cells. In summary, our findings suggested that NSCLCAT1 potentially has a role in NSCLC and NSCLCAT1-mediated regulation of the Hippo signaling pathway through the transcriptional repression of CDH1; therefore, the functional suppression or inhibition of NSCLCAT1 could be used as a novel therapeutic pathway in the control of aggressive and metastatic NSCLC.-Zhao, W., Zhang, L.-N., Wang, X.-L., Zhang, J., Yu, H.-X. Long noncoding RNA NSCLCAT1 increases non-small cell lung cancer cell invasion and migration through the Hippo signaling pathway by interacting with CDH1.

MicroRNA-384 inhibits the progression of esophageal squamous cell carcinoma through blockade of the LIMK1/cofilin signaling pathway by binding to LIMK1.

INTRODUCTION: Esophageal squamous cell carcinoma (ESCC) represents an aggressive malignancy often accompanied with a poor prognosis. Owing to the poor mortality and morbidity rates associated with this malignancy, a deeper understanding of the finer molecular changes that occur in ESCC is required in order to identify novel potential targets for early detection and therapy. At present the mechanism by which ESCC functions on a molecular level is not fully understood. Hence, the aim of the present study was to ascertain as to whether microRNA-384 (miR-384) influences the progression of ESCC. MATERIAL AND METHODS: Bioinformatics analysis was initially conducted to identify ESCC-related differentially expressed genes and predict regulatory miRs. After the target relationship between miR-384 and LIMK1 had been verified, the expression of miR-384 and LIMK1 in the EC9706 cell line was altered in an attempt to investigate the regulatory roles of miR-384 in the expression of the LIMK1/cofilin signaling pathway-related genes, cell proliferation, invasion, cell cycle distribution and apoptosis, in addition to lymph node metastasis (LNM) and tumor growth in nude mice. RESULTS: Microarray-based gene expression profiling indicated that miR-384 affected the progression of ESCC through the LIMK1-mediated LIMK1/cofilin signaling pathway. Furthermore, miR-384 and Bax were observed to be poorly expressed, while LIMK1, cofilin and Bcl-2 were highly expressed in ESCC. The obtained evidences indicating that miR-384 targeted and negatively regulated LIMK1. Upregulation of miR-384 or LIMK1 inhibition was determined to block the LIMK1/cofilin signaling pathway, repress cell proliferation, invasion, cell cycle, LNM and tumor growth, while promote cell apoptosis in ESCC. CONCLUSION: Collectively, based on the key findings of the study, miR-384 could sequester LIMK1, which acts to suppress activation of the LIMK1/cofilin signaling pathway, thus ultimately inhibiting the development and progression of ESCC.

Involvement of the TLR4/NF-κB Signaling Pathway in the Repair of Esophageal Mucosa Injury in Rats with Gastroesophageal Reflux Disease.

BACKGROUND/AIMS: Numerous studies have highlighted the activation of NF-κB in the esophageal mucosa during the early stages of gastroesophageal reflux disease (GERD). The present study aimed to investigate the role of the TLR4/NF-κB signaling pathway in GERD rat models. METHODS: Wistar rats (n = 60) were recruited to establish a GERD animal model. Distal esophageal pH was assessed, followed by determination of the contents of thiobarbituric acid-reactive species (TBARS) and reactive oxygen species (ROS) in esophageal mucosa homogenate. ELISA was employed to detect the levels of inflammatory factors (IL-6, IL-8, IL-10 and TNF-α) in esophageal mucosa. The expression of MMP-3, MPP-9, Cldn1 and Cldn4 was determined by immunohistochemistry. RT-qPCR and western blot analysis were applied to evaluate the protein expressions in TLR4/NF-κB signaling pathway, while TUNEL staining was utilized to examine the apoptosis rate in the esophageal mucosal tissues. RESULTS: Distal esophageal pH of the rats was higher in the GERD + PDTC group than in other groups. Levels of inflammatory factors in esophageal mucosal tissues were downregulated with the inhibition of NF-κB, which was determined to be associated with the decreased contents of TBARS and ROS. Moreover, decreased MMP-3 and MPP-9 in addition to elevated Cldn1 and Cldn4 were detected in the esophageal mucosa as a result of the inactivation of NF-κB. The TLR4/NF-κB signaling pathway-related proteins (TLR4, NF-κB and IκBα); the rate of apoptosis was demonstrated to be suppressed in the GERD + PDTC group, while inactivating NF-κB was found to alleviate the tissue damage observed in the esophageal mucosa. CONCLUSION: The key findings of the current study demonstrate that the inactivation of the TLR4/NF-κB signaling pathway alleviates oxidative stress injury and promotes the repair of esophageal mucosal injury among rats with GERD, highlighting a potential novel GERD mechanism.

Esophageal hiatal hernia: risk, diagnosis and management.

INTRODUCTION: Esophageal hiatal hernia involves abnormal abdominal entry into thoracic cavity. It is classified based on orientation between esophageal junction and diaphragm. Sliding hiatal hernia (Type-I) comprises the most frequent category, emanating from right crus of diaphragm. Type-II esophageal hernia engages both left and right muscular crura. Type-III and IV additionally include the left crus. Age and increased body mass index are key risk factors, and congenital skeletal aberrations trigger pathogenesis through intestinal malrotations. Familiar manifestations include gastric reflux, nausea, bloating, chest and epigastric discomfort, pharyngeal and esophageal expulsion and dysphagia. Weight loss and colorectal bleeding are severe symptoms. Areas covered: This review summarizes updated evidence of pathophysiology, risk factors, diagnosis and management of hiatal hernias. Laparoscopy and oesophagectomy procedures have been discussed as surgical procedures. Expert commentary: Endoscopy identifies untreatable gastric reflux; radiology is better for pre-operative assessments; manometry measures esophageal peristalsis, and CT scanning detects gastric volvulus and associated organ ruptures. Gastric reflux disease is mitigated using antacids and proton pump and histamine-2-receptor blockers. Severe abdominal penetration into chest cavity demands surgical approaches. Hence, esophagectomy has chances of post-operative morbidity, while minimally invasive laparoscopy entails fewer postoperative difficulties and better visualization of hernia and related vascular damages.

The integrated quality assessment of Chinese commercial dry red wine based on a method of online HPLC-DAD-CL combined with HPLC-ESI-MS.

AIM: To apply an integrated quality assessment strategy to investigate the quality of multiple Chinese commercial dry red wine samples. METHOD: A comprehensive method was developed by combining a high performance liquid chromatography-diode array detector-chemiluminescence (HPLC-DAD-CL) online hyphenated system with an HPLC-ESI-MS technique. RESULTS: Chromatographic and H2O2-scavenging active fingerprints of thirteen batches of different, commercially available Chinese dry red wine samples were obtained and analyzed. Twenty-five compounds, including eighteen antioxidants were identified and evaluated. The dominant and characteristic antioxidants in the samples were identified. The relationships between antioxidant potency and the cultivated variety of grape, producing area, cellaring period, and trade mark are also discussed. CONCLUSION: The results provide the feasibility for an integrated quality assessment strategy to be efficiently and objectively used in quality (especially antioxidant activity) assessment and identification of dry red wine.

Qualitative and quantitative analysis of phenolic compounds in the leaves of aquilaria sinensis using liquid chromatography-mass spectrometry.

INTRODUCTION: The leaves of Aquilaria sinensis traditionally have been used in China for a century. Phenolic compounds were investigated to be the major active compounds in them. OBJECTIVE: To establish a method that will simultaneously determine the phenolic compounds in Aquilaria sinensis leaves and identify their characteristic fragmentation patterns, and to make a comparison of A. sinensis leaf samples from different areas of China. METHODS: High-performance liquid chromatography (HPLC) coupled with mass spectrometry (MS) and photodiode array detection (DAD) were used for the qualitative and quantitative analysis. RESULTS: Twenty-one compounds, including xanthones, benzophenones and flavones, were identified or tentatively characterised. The fragmentation patterns of xanthones and benzophenones were also described. Also, eight components in the herbal samples from different regions were determined by HPLC-DAD. CONCLUSION: The method developed is suitable for the qualitative and quantitative analysis of phenolic constituents in the leaves of A. sinensis.