Current Issue : October - December Volume : 2013 Issue Number : 4 Articles : 5 Articles
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Researchers are looking into the potential development of natural compounds for anticancer therapy. Previous studies have\r\npostulated the cytotoxic effect of helichrysetin towards different cancer cell lines. In this study, we investigated the cytotoxic\r\neffect of helichrysetin, a naturally occurring chalcone on four selected cancer cell lines, A549, MCF-7, Ca Ski, and HT-29, and\r\nfurther elucidated its biochemical and molecular mechanisms in human lung adenocarcinoma, A549. Helichrysetin showed the\r\nhighest cytotoxic activity against Ca Ski followed by A549. Changes in the nuclear morphology of A549 cells such as chromatin\r\ncondensation and nuclear fragmentation were observed in cells treated with helichrysetin. Further evidence of apoptosis includes\r\nthe externalization of phosphatidylserine and the collapse of mitochondrial membrane potential which are both early signs of\r\napoptosis. These signs of apoptosis are related to cell cycle blockade at the S checkpoint which suggests that the alteration of the cell\r\ncycle contributes to the induction of apoptosis in A549.These results suggest that helichrysetin has great potentials for development\r\nas an anticancer agent....
Spontaneous pneumothorax, a prevalent medical challenge in most trauma cases, is a formof sudden lung collapse closely associated\r\nwith risk factors such as lung cancer and emphysema. Our work seeks to explore and quantify the currently unknown pathological\r\nfactors underlying lesion rupture in pneumothorax through biomechanical modeling. We hypothesized that lesion instability is\r\nclosely associated with elastodynamic strain of the pleural membrane from pulsatile air flow and collagen-elastin dynamics. Based\r\non the principles of continuummechanics and fluid-structure interaction, our proposedmodel coupled isotropic tissue deformation\r\nwith pressure from pulsatile air motion and the pleural fluid. Next, we derived mathematical instability criteria for our ordinary\r\ndifferential equation system and then translated these mathematical instabilities to physically relevant structural instabilities via\r\nthe incorporation of a finite energy limiter. The introduction of novel biomechanical descriptions for collagen-elastin dynamics\r\nallowed us to demonstrate that changes in the protein structure can lead to a transition from stable to unstable domains in the\r\nmaterial parameter space for a general lesion. This result allowed us to create a novel streamlined algorithm for detecting material\r\ninstabilities in transient lung CT scan data via analyzing deformations in a local tissue boundary....
Background: Although granulomatous inflammation is a central feature of many disease processes, cellular\r\nmechanisms of granuloma formation and persistence are poorly understood. Carbon nanoparticles, which can be\r\nproducts of manufacture or the environment, have been associated with granulomatous disease. This paper utilizes\r\na previously described carbon nanoparticle granuloma model to address the issue of whether peroxisome\r\nproliferator-activated receptor gamma (PPAR?), a nuclear transcription factor and negative regulator of inflammatory\r\ncytokines might play a role in granulomatous lung disease. PPAR? is constitutively expressed in alveolar\r\nmacrophages from healthy individuals but is depressed in alveolar macrophages of patients with sarcoidosis, a\r\nprototypical granulomatous disease. Our previous study of macrophage-specific PPAR? KO mice had revealed an\r\nintrinsically inflammatory pulmonary environment with an elevated pro-inflammatory cytokines profile as compared\r\nto wild-type mice. Based on such observations we hypothesized that PPAR? expression would be repressed in\r\nalveolar macrophages from animals bearing granulomas induced by MWCNT instillation.\r\nMethods: Wild-type C57Bl/6 and macrophage-specific PPAR? KO mice received oropharyngeal instillations of\r\nmultiwall carbon nanotubes (MWCNT) (100 �µg). Bronchoalveolar lavage (BAL) cells, BAL fluids, and lung tissues were\r\nobtained 60 days post-instillation for analysis of granuloma histology and pro-inflammatory cytokines (osteopontin,\r\nCCL2, and interferon gamma [IFN-?] mRNA and protein expression.\r\nResults: In wild-type mice, alveolar macrophage PPAR? expression and activity were significantly reduced in\r\ngranuloma-bearing animals 60 days after MWCNT instillation. In macrophage-specific PPAR? KO mice, granuloma\r\nformation was more extensive than in wild-type at 60 days after MWCNT instillation. PPAR? KO mice also\r\ndemonstrated elevated pro-inflammatory cytokine expression in lung tissue, laser-microdissected lung granulomas,\r\nand BAL cells/fluids, at 60 days post MWCNT exposure.\r\nConclusions: Overall, data indicate that PPAR? deficiency promotes inflammation and granuloma formation,\r\nsuggesting that PPAR? functions as a negative regulator of chronic granulomatous inflammation....
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