Anomalous systemic arterial supply to the left lower lung lobe: A case report.

Background: An anomalous systemic arterial supply to the lung lobes is a rare congenital pulmonary vascular malformation. Current treatments include thoracoscopic lobectomy, anatomical segmentectomy, simple ligation and arterial embolization. However, the optimal treatment remains controversial. Case presentation: A 29-year-old man was diagnosed with anomalous systemic arterial supply to the left lower lobe through contrast-enhanced computed tomography and three-dimensional reconstruction. He underwent coil embolization of the anomalous artery and was followed up for 1 year. Conclusions: Blockage of the blood flow of the anomalous systemic artery alone does not improve the blood supply of the pulmonary artery to lung tissue and thus cannot restore normal gas exchange through the blood-gas barrier. Coil embolization of the anomalous arterial supply can cause early postoperative pulmonary infarction.

Roles of Nrf2/HO-1 and HIF-1α/VEGF in lung tissue injury and repair following cerebral ischemia/reperfusion injury.

Cerebral ischemia/reperfusion injury (CIRI) leads to injury in distant organs, most commonly the lungs, although limited studies have examined self-protective mechanisms during CIRI-induced lung injury. Here, we investigated self-protective mechanisms that attenuate stress-related injury and promote the angiogenetic repair of epithelial function during CIRI-induced lung injury by measuring nuclear factor erythroid-related factor 2 (Nrf2) and hypoxia-inducible factor-1α (HIF-1α) levels. A CIRI model was established in male Sprague-Dawley rats by blocking the middle cerebral artery. Rats were divided into five subgroups based on the reperfusion time (6, 12, 24, 48, and 72 hr). Lung injury was assessed using a semiquantitative score and a thiobarbituric acid-based method of determining malonaldehyde production. Lung tissue angiogenesis was detected by CD34 and CD31 immunolabeling. Changes in Nrf2, heme oxygenase-1 (HO-1), HIF-1α, vascular-endothelial growth factor (VEGF), phosphatidylinositol 3-kinase (PI3K), extracellular-regulated kinase1/2 (ERK1/2), and phospho-ERK1/2 ( p-ERK1/2) protein- and mRNA-expression levels were measured by immunohistochemistry and reverse transcription polymerase chain reactions, respectively. Oxidative stress induced by cerebral ischemia/reperfusion (CI/R) caused lung injury. Expression of the Nrf2/HO-1 antioxidative stress pathway in lung tissues increased following CI/R, peaking after 24 hr. PI3K, ERK, and p-ERK1/2, which act upstream of Nrf2/HO-1, were expressed at higher levels in the CI/R-model group, consistent with the general trends observed for Nrf2/HO-1. Within 72 hr post-CI/R, HIF-1α, and VEGF expression significantly increased versus the sham group. Thus, during CIRI-induced lung injury, the body may upregulate antioxidative stress activities and promote angiogenesis to repair the endothelial barrier through the Nrf2/HO-1 and HIF-1α/VEGF signaling pathways, enabling self-protection.

Serum Fork-Head Box D3 (FOXD3) Expression Is Down-Regulated in and Associated with Diagnosis of Patients with Non-Small Cell Lung Cancer.

BACKGROUND The aim of this study was to detect the expression of fork-head box D3 (FOXD3) and investigate its diagnostic value in patients with non-small cell lung cancer (NSCLC). MATERIAL AND METHODS The relative expression of FOXD3 at mRNA and protein levels was determined by quantitative reverse transcription polymerase chain reaction (qRT-PCR) and Western blotting analysis, respectively. Chi-square test was used to explore the relevance of FOXD3 expression with clinical features of NSCLC patients. A receiver operating characteristic (ROC) curve was built to estimate the diagnostic value of FOXD3 in distinguishing NSCLC patients from healthy controls. RESULTS Serum FOXD3 expression was weakly expressed in NSCLC patients compared to the controls at mRNA and protein levels (P<0.001) and low FOXD3 expression was positively correlated with TNM stage, lymph node metastasis, and differentiation. The ROC curve indicated that FOXD3 acts as a diagnostic bio-marker for NSCLC patients, with an AUC of 0.826 corresponding to a sensitivity of 77.1% and a specificity of 74.6%, and an optimal cutoff point of 2.38. CONCLUSIONS Decreased expression of serum FOXD3 was observed in NSCLC patients, and it was found to be a potential molecular marker for the diagnosis of NSCLC.

Cerebral ischemia/reperfusion injury induces airway mucus hypersecretion in rats and activates IL­13­associated inflammatory mechanisms.

The majority of patients that suffer a stroke have excessive sputum, which accelerates the development of pulmonary complications. However, it is unclear whether cerebral ischemia and reperfusion (I/R) injury induces mucus hypersecretion, and the potential role of inflammation remains unknown. In the present study, the reversible middle cerebral artery occlusion model was applied in rats to induce cerebral I/R injury. The rats were grouped according to the duration of reperfusion (6, 12, 24, 48 and 72 h). Neurological dysfunction was evaluated by Longa scoring and lung dry­to­wet weight (dw/ww) ratios were determined to reflect the degree of mucus secretion. Inflammatory factor interleukin­13 (IL­13) and tumor necrosis factor­α (TNF­α) levels in serum and bronchoalveolar lavage fluid (BALF) were determined by enzyme­linked immunosorbent assay. Pulmonary levels of mucin 5AC (MUC5AC) and key molecules involved in nuclear factor­κB (NF­κB) signaling were determined by western blotting and immunohistochemistry. Rats with cerebral I/R had impaired neurological function, which was associated with the length of reperfusion time. In addition, the dw/ww lung ratio decreased and the pulmonary expression of MUC5AC increased with the increase in severity of neurological dysfunction, indicating that cerebral I/R may induce mucus hypersecretion in a reperfusion time­dependent manner. IL­13 and TNF­α levels in serum and BALF, as well as the nuclear translocation of NF­κB p65 in pulmonary tissues, significantly increased following cerebral I/R, which suggests that the activation of IL­13 and NF­κB inflammatory pathways may be involved. The present study concluded that cerebral I/R injury may induce airway mucus hypersecretion by activating IL­13 and NF­κB inflammatory pathways.

Long non-coding RNA BANCR promotes proliferation and migration of lung carcinoma via MAPK pathways.

Lung carcinoma (LC) is one of the most mortal malignant tumors, and is becoming one of most lethal threat to human health and life. LncRNAs, emerging non-coding RNAs but poorly understood, are involved in the proliferation, metastasis, infiltration and apoptosis of LC. In this study, an lncRNA BANCR in LC cells was chosen to investigate the effect on LC cells, and clarify the possible mechanism. The results showed that BANCR levels were downregulated in LC cells. When BANCR expression was improved by tranfection with pcDNA-BANCR vector, tumor growth was suppressed. Vise versa, when BANCR was knockdown by si-BANCR, cell proliferation and migration of LC were remarkably promoted. We further found that MAPK pathways were involved in the BANCR-mediated cell proliferation and migration of LC. Moreover, BANCR was found to regulate LC proliferation and migration via not ERK MAPK, but p38 MAPK and JNK inactivations. These findings not only suggested that BANCR may be a new target for LC chemotherapy in future, but also will help us to fully understand the oncogenesis of LC.