Saccadic suppression: elevation of visual threshold associated with saccadic eye movements.
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Biomedical subjects
Publications and source records attributed to L Stark.
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The maximum velocities of microsaccades (flicks) are an increasing function of amplitude of movement. Measured velocities fall on the extrapolation of the curve of maximum velocity versus amplitude for voluntary saccades and involuntary corrective saccades. Hence all these movements are produced by a common physiological system, or the characteristics of the movements are determined by a single dynamically limiting element.
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BACKGROUND: Tumour necrosis factor (TNF)-alpha has considerable anti-tumour activity and may have potential as a treatment for metastatic colorectal cancer. However, TNF-alpha responses in patients and cell lines are variable and TNF-alpha treatment is associated with dose limiting clinical toxicity. Activation of NF-kappaB is protective against TNF-alpha induced cell death, and this may explain tumour resistance. METHODS: In order to provide further understanding of determinants of TNF-alpha responses, we studied TNF-alpha induced NF-kappaB activation and variable tumour responses. We analysed the kinetics of TNF-alpha induced NF-kappaB activation in colorectal cancer cells and determined whether it is possible to sensitize colorectal tumour cells to TNF-alpha by modulation of NF-kappaB signalling. RESULTS: We demonstrated that sustained NF-kappaB activation exceeding 16 h was observed in HRT18 and SW480 cells and was associated with TNF-alpha resistance. In contrast, transient NF-kappaB activation in HCT116 cells was associated with sensitivity to cytotoxic TNF-alpha effects, suggesting that NF-kappaB kinetics may have utility as clinical marker of TNF-alpha tumour resistance. Despite variable TNF-alpha responses and NF-kappaB kinetics, all three colorectal cancer cell lines were highly sensitive to treatment with the TNF-related apoptosis-inducing ligand (TRAIL) which induced only transient NF-kappaB activation. This further supports the notion of a pre-determined NF-kappaB response influencing receptor-mediated cell death. We also show that stable transfection and adenoviral-mediated expression of IkappaB(A32/36) can be used to confer TNF-alpha sensitivity to colorectal tumour cells previously resistant. CONCLUSIONS: These findings indicate that a combined approach using gene therapy and recombinant TNF-alpha merits further appraisal. Furthermore, the kinetics of the TNF-alpha response could be determined using a 'test-dose' to indicate whether individual patients might benefit from this gene therapy approach.
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Two field studies were conducted at a research station in Tampa, Florida to assess the removal of bacteriophage PRD1 from wastewater in septic tank drainfields. Infiltration cells were seeded with PRD1 and bromide and the effects of effluent hydraulic loading rate and rainfall on virus removal were monitored. Septic tank effluent samples were collected after passage through 0.6 m of unsaturated fine sand and PRD1 was detected over an average of 67 d. Bacteriophage PRD1 breakthrough was detected at approximately the same time as bromide in all three cells except for the low-load cell (Study 1), where bromide was never detected. Log10 removals of PRD1 were 1.43 and 1.91 for the high-load cells (hydraulic loading rate = 0.063 m/d) and 2.21 for the low-load cell (hydraulic loading rate = 0.032 m/d). Virus attenuation is attributed to dispersion, dilution, and inactivation. Significant increases in PRD1 elution with rainfall were observed in the first 10 d of the study. Approximately 125 mm of rainfall caused a 1.2 log10 increase of PRD1 detected at the 0.6-m depth. Current Florida onsite wastewater disposal standards, which specify a 0.6-m distance from the drainfield to the water table, may not provide sufficient removal of viruses, particularly during the wet season.
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