The Role of Hydrogen Sulfide in the Development and Progression of Lung Cancer.

Lung cancer is one of the 10 most common cancers in the world, which seriously affects the normal life and health of patients. According to the investigation report, the 3-year survival rate of patients with lung cancer is less than 20%. Heredity, the environment, and long-term smoking or secondhand smoke greatly promote the development and progress of the disease. The mechanisms of action of the occurrence and development of lung cancer have not been fully clarified. As a new type of gas signal molecule, hydrogen sulfide (H2S) has received great attention for its physiological and pathological roles in mammalian cells. It has been found that H2S is widely involved in the regulation of the respiratory system and digestive system, and plays an important role in the occurrence and development of lung cancer. H2S has the characteristics of dissolving in water and passing through the cell membrane, and is widely expressed in body tissues, which determines the possibility of its participation in the occurrence of lung cancer. Both endogenous and exogenous H2S may be involved in the inhibition of lung cancer cells by regulating mitochondrial energy metabolism, mitochondrial DNA integrity, and phosphoinositide 3-kinase/protein kinase B co-pathway hypoxia-inducible factor-1α (HIF-1α). This article reviews and discusses the molecular mechanism of H2S in the development of lung cancer, and provides novel insights for the prevention and targeted therapy of lung cancer.

Automatic characterization of classic choroidal neovascularization by using AdaBoost for supervised learning.

PURPOSE: To provide a computer-aided visualization tool for accurate diagnosis and quantification of choroidal neovascularization (CNV) on the basis of fluorescence leakage characteristics. METHODS: All image frames of a fluorescein angiography (FA) sequence are first aligned and mapped to a global space. To automatically determine the severity of each pixel in the global space and hence the extent of CNV, the system matches the intensity variation of each set of spatially corresponding pixels across the sequence with the targeted leakage pattern, learned from a sampled population graded by a retina specialist. The learning strategy, known as the AdaBoost algorithm, has 12 classifiers for 12 features that summarize the variation in fluorescence intensity over time. Given a new sequence, the severity map image is generated using the contribution scores of the 12 classifiers. Initialized with points of low and high severity, regions of CNV are delineated using the random walk algorithm. RESULTS: A dataset of 33 FA sequences of classic CNV showed the average accuracy of CNV delineation to be 83.26%. In addition, the 30- to 60-second interval provided the most reliable information for differentiating CNV from the background. Using eight sequences of multiple visits of four patients for evaluation of the postphotodynamic therapy (PDT), the statistics derived from the segmented regions correlate closely with the clinical observed changes. CONCLUSIONS: The clinician can easily visualize the temporal characteristics of CNV fluorescence leakage using the severity map, which is a two-dimensional summary of a complete FA sequence. The computer-aided tool allows objective evaluation and computation of statistical data from the automatic delineation for surgical assessment.

Requirement of inducible nitric-oxide synthase in lipopolysaccharide-mediated Src induction and macrophage migration.

Previously, we have demonstrated the induction of Src in lipopolysaccharide (LPS)-stimulated macrophages. In this study, we observed that pharmacological blockade or knockout of inducible nitric-oxide synthase (iNOS) reduced LPS-mediated Src induction and macrophage migration. Either SNAP (a NO donor) or 8-Br-cGMP (a cGMP analogue) could rescue these defects in iNOS-null macrophages, which indicated the participation of NO/cGMP in LPS-elicited Src expression and mobilization. In addition, Src family kinase (SFK)-specific inhibitor, PP2, inhibited SNAP- and 8-Br-cGMP-evoked motility implicating the involvement of SFKs downstream of NO/cGMP. Analysis of the expression of SFKs indicated LPS dramatically induced Src, which could be attributable to the increased level of the src transcript. Attenuation of Src by src-specific siRNA reduced LPS- and SNAP-evoked mobilization in Raw264.7 macrophages, and reintroduction of avian Src could rescue their motility. Furthermore, LPS-mediated Src induction led to increased FAK Pi-Tyr-397 and Pi-Tyr-861, which was also iNOS-dependent. With these findings, we concluded that iNOS was important for LPS-mediated macrophage locomotion and Src was a critical player in this process.