Changes In Submersed Macrophytes In Relation To Tidal Storm Surges

We analyzed long-term submersed macrophyte presence-absence data collected from 15 stations in Kings Bay/Crystal River, Florida in relation to three major storm events. The percent occurrence of most species declined immediately after storm events but the recovery pattern after the storm differed among species. Hydrilla (Hydrilla verticillata (L.F.) Royle)and Eurasian watermilfoil (Myriophyllum spicatum L.) exhibited differing recolonization behaviors. Eurasian watermilfoil recolonized quickly after storms but declined in abundance as hydrilla began to increase in abundance. Natural catastrophic events restructure submersed macrophyte communities by eliminating the dominate species, and allowing revegetation and restructuring of communities. Tidal surges may also act to maintain species diversity in the system. In addition, catastrophic events remove dense nuisance plant growth for several years, altering the public's perception of the nuisance plant problem of Kings Bay/Crystal River

phase i ii study of spartalizumab pdr001 an anti pd1 mab in patients with advanced melanoma or non small cell lung cancer

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Silencing of IQGAP1 by shRNA inhibits the invasion of ovarian carcinoma HO-8910PM cells in vitro

<p>Abstract</p> <p>Background</p> <p>IQGAP1 is a scaffolding protein and overexpressed in many human tumors, including ovarian cancer. However, the contribution of IQGAP1 to invasive properties of ovarian cancer cells remains unknown. Here, we investigated the effect of IQGAP1-specific short hairpin RNA (shRNA) expressing plasmids on metastatic potential of ovarian cancer HO-8910PM cells.</p> <p>Methods</p> <p>We used RT-PCR and Western blot analysis to characterize expression of IQGAP1 in three human ovarian cancer-derived cell lines SK-OV-3, HO-8910 and HO-8910PM. We then determined whether expression of endogenous IQGAP1 correlated with invasive and migratory ability by using an in vitro Matrigel assay and cell migration assay. We further knocked down IQGAP1 using shRNA expressing plasmids controlled by U1 promoter in HO-8910PM cells and examined the proliferation activity, invasive and migration potential of IQGAP1 shRNA transfectants using MTT assay, in vitro Matrigel-coated invasion assay and migration assay.</p> <p>Results</p> <p>IQGAP1 expression level seemed to be closely associated with the enhanced invasion and migration in ovarian cancer cell lines. Levels of both IQGAP1 mRNA and protein were significantly reduced in HO-8910PM cells transfected with plasmid-based IQGAP1-specific shRNAs. RNAi-mediated knockdown of IQGAP1 expression in HO-8910PM cells resulted in a significant decrease in cell invasion and migration.</p> <p>Conclusion</p> <p>Our findings support the hypothesis that IQGAP1 promotes tumor progression and identify IQGAP1 as a potential therapeutic strategy for ovarian cancer and some other tumors with over-expression of the IQGAP1 gene.</p

MALDI-MSI and label-free LC-ESI-MS/MS shotgun proteomics to investigate protein induction in a murine fibrosarcoma model following treatment with a vascular disrupting agent

Tumour vasculature is notoriously sinusoidal and leaky, and is hence susceptible to vascular disruption. Microtubule destabilising drugs such as the combretastatins form the largest group of tumour vascular disrupting agents (VDAs) and cause selective shutdown of tumour blood flow within minutes to hours, leading to secondary tumour cell death. Targeting the tumour vasculature is a proven anticancer strategy but early treatment response bio-markers are required for personalising treatment planning. Protein induction following treatment with combretastatin A4-phosphate (CA4P) was examined in a mouse fibrosarcoma model (fs 188), where tumour cells express only the matrix-bound isoform of vascular endothelial growth factor A (VEGF188). These tumours are relatively resistant to vascular disruption by CA4P and hence a study of protein induction following treatment could yield insights into resistance mechanisms. The distribution of a number of proteins induced following treatment were visualised by MALDI-MSI. Responses identified were validated by LC-ESI-MS/MS and immunohistochemical (IHC) staining. Significant changes in proteins connected with necrosis, cell structure, cell survival and stress-induced molecular chaperones were identified. Protein-protein interactions were identified using STRING 9.0 proteomic network software. These relationship pathways provided an insight into the activity of the active tumour milieu and a means of linking the identified proteins to their functional partners