Seeing by exploring

The classical notion of how things are seen is that perception is passive, that the eyes are windows, and in floods reality. Physiological work of the 19th century cast doubt on this view that perception is passive acceptance of reality. Perception is not at the present time a popular topic for philosophers. This must be partly because scientific accounts of perception have now gone a long way away from appearances. They depend on physiological and psycho-physical experiments which require technical investigation and do not fall within traditional concepts of philosophy. Theories of visual perception are examined, both from a physical and psycho-physical standpoint

Nicotine Effects Surface Bound Enolase on Streptococcus mutans and Its Binding to Human Plasminogen

poster abstractStreptococcus mutans is the major bacterial agent responsible for dental caries. Previous research has shown that smokers have increased caries and that nicotine increases biofilm formation of S. mutans. S. mutans is also associated with atherosclerosis, another disease commonly found in smokers. However, little research has been done to investigate the direct effect of nicotine on the ability of S. mutans to bind to endothelial cells and lead to atherosclerosis. The two objectives of this study were to determine how nicotine affects the level of enolase, a glycolytic enzyme, on the surface of S. mutans, and next to determine its effect on binding of treated bacteria to human plasminogen, a protein present in the bloodstream. S. mutans strain UA159 was grown overnight in tryptic soy broth treated with 0, 0.5, 1, and 2 mg/mL nicotine at 37◦C in 5% CO2. These cells were used to coat a microtiter plate, and various levels of surface bound enolase and binding to plasminogen were determined using enzyme-linked immunosorbent assays (ELISA). A preliminary trial showed increase in both surface bound enolase and binding to plasminogen with increasing nicotine concentration. Similar results are to be expected with repetition of this procedure, indicating that nicotine up-regulates the bacterial expression of enolase and its binding to plasminogen, probably through plasminogen binding receptors, contributing to the virulence of S. mutans. Knowledge of the attachment mechanisms of S. mutans in the presence of tobacco may aid in prevention of tobacco-related atherosclerosis

Determining The Effects of Fulvic acid on Biofilm/Planktonic Streptococcus Mutans Growth

poster abstractFulvic acid, a major organic compound extract of Shilajit has been the focus of dental research for the past few years. Shilajit, a sticky tar-like substance of dark brownish color, was used during the ancient times, thousands of years ago and continues to be the traditional method today in India to aid with curing bone/cartilage diseases. Shilajit has also been proven to have anti-inflammatory and pain suppressing effects. This experiment determined the minimum inhibitory concentration (MIC), which is the lowest concentration of fulvic acid, an active component of shilajit that inhibits the visible growth of S. mutans. This experiment also determined the minimum bactericidal concentration (MBC) which is the lowest concentration of fulvic acid that kills S. mutans. A 3-day procedure to determine the growth vs inhibition of the S. mutans was conducted and bacterial readings were recorded using a spectrophotometer after treating S. mutans with 10% formaldehyde, crystal violet stain, and iso-propanol with 30-45 minute incubations between each. The experiment determined that very high concentrations of fulvic acid killed S. mutans, while less concentrated fulvic acid inhibited the growth of S. mutans bacterial cells. A solution comprised of a 5% concentration of fulvic acid killed all of the S. mutans; 5.00%, 2.50%, and 1.25% fulvic acid concentrations had bacterial absorbance of 0.000, 0.009, and 0.027, respectively, as compared to the control group’s normal bacterial growth absorbance of 0.254. Additionally, solutions ranging from a two-fold dilution of fulvic acid to six-fold dilution of fulvic acid inhibited the growth of S. mutans. A similar trend was also observed in planktonic and biofilm formation. For all of the above, in the seventh and eighth dilution (0.078% and 0.039% respectively) of the fulvic acid, the growth of S. mutans bacteria was similar to the control group due to the level of dilution. Overall it was observed that fulvic acid is able to kill bacteria in strong concentrations. Additionally it is able to inhibit further growth of bacteria in lower concentrations, but once the solution becomes too dilute, it does not have an effect on bacterial growth. This contributes greatly to the field of oral health because this data can be utilized for further research on oral bacterial growth inhibitors. Furthermore, the data collected here is a significant starting point for research on the specific minimum concentrations necessary to inhibit oral bacteria growth, because this can be used to determine the smallest amounts of fulvic acid, the bacteria the human body can handle

Effect of Nicotine on Planktonic and Biofilm Growth Phases of an Experiment

poster abstractTobacco and cigarette smoke increase the risk of periodontal disease, one of the most widespread human diseases. It has been established that Porphormonas gingivalis, a gram negative anaerobic bacterium, is one of the main causative agents of periodontal disease. Prior research indicates that P. gingivalis binds to Fusobacterium nucleatum in oral biofilms. It is not yet understood if nicotine, a major component of cigarette smoke, affects the growth of bacteria differently if added in the planktonic phase, defined as the primary subculture from agar to broth before the start of a biofilm formation experiment, or the biofilm phase, defined as the secondary subculture from broth culture to a microtiter plate. Therefore, the main objective of this study is to understand this methodological difference. F. nucleatum and P. gingivalis were both grown in anaerobic GasPak containers on blood agar plates. The media for primary subculture consisted of a Brain Heart Infusion (BBL) broth supplemented with 5 g/L yeast extract and 5% vitamin K & hemin serum at 37oC. F. nucleatum was subcultured in the absence of nicotine and plated on a 96 well plate to establish biofilm. P. gingivalis was subcultured in varying concentrations of nicotine and subcultured on top of the F. nucleate biofilm. Biofilm mass was analyzed using the crystal violet technique and samples were measured in a spectrophotometer at 490 nm. The results demonstrated a statistically significant increase in biofilm formation when P. gingivalis was subjected to a higher nicotine concentration in the planktonic phase in comparison to a lower nicotine concentration in the biofilm phase. This data suggests a nicotine assisted activation of receptors on the surface of P. gingivalis specific for binding to F. nucleatum. Further testing on the receptors through a biotinylation assay will confirm the results

“Open Markets” v. “Structured Bilateral Trades”: Results of Economic Modeling of Point-to-Point Source Water Quality Trading in the Non-Tidal Passaic River Basin

Environmental Economics and Policy,

Serotype k Streptococcus mutans Binding to Collagen and Fibrinogen in Nicotine

poster abstractBackground: Streptococcus mutans is a gram-positive coccus-shaped, facultatively anaerobic bacterium that is commonly found in the human oral cavity and is a major contributor to tooth decay. The bacterium has the potential to make its way into the blood stream and adhere to endothelial cell proteins such as collagen and fibrinogen in the arteries through specific receptors potentially leading to atherosclerosis. Endothelial cells secrete cell-associated and cell-free collagen and fibrinogen. Specifically, serotype k S. mutans have been associated with atherosclerosis and nicotine has been shown to increase the biofilm formation of S. mutans (serotype k). The focus of this research was to measure S. mutans ability to bind to collagen type I and fibrinogen when the cells were grown in the presence of nicotine. Methods: S. mutans serotype k strains 51, 52, and 89 were cultured in 0–2 mg/mL nicotine. Formaldehyde was added to kill the cells followed by labeling the cells with biotin. Collagen type I and fibrinogen were coated (1 μg/mL) onto 96-well microtiter plates. The plates were washed and 1% BSA was added to block the wells. Then the biotinylated nicotine-treated S. mutans were added, incubated to allow binding to the endothelial cell proteins, and washed. Finally, ExtrAvidin HRP and OPD were added to the plate and the optical density was measured at an absorbance of 490 nm. Results: The optical density was directly related to the relative number of cells bound to collagen type I and fibrinogen. Conclusion: The results demonstrated a significant increase in all three strains of S. mutans binding to the proteins when cultured in 1 and 2 mg/mL concentrations of nicotine compared to the 0 nicotine control. The increased numbers of nicotine-treated S. mutans binding to the endothelial cell proteins may have the ability to contribute to atherosclerosis

Nicotine Kill Time of Streptococcus Mutans

poster abstractCigarettes have thousands of components aside from tobacco and nicotine that are harmful to the smoker’s body. Smoking is considered a significant risk factor for cardiovascular disease (CVD) and periodontal disease. Yet smoking also plays a significant role in the buildup of plaque in the mouths of smokers. This is in part due to the formation of biofilm by Streptococcus mutans. S. mutans is an oral bacterium found in most humans that is considered to be the causative agent for dental caries. Particularly, S. mutans UA159 was used in this experiment. Biofilm formation regarding S. mutans and nicotine concentrations has previously been studied. It was found that at high concentrations of nicotine, biofilm formation of S. mutans decreased significantly. One of the aims of this study is to determine the time required to kill S. mutans

Streptococcus mutans Binding to Collagen, Fibrinogen, Fibronectin, and Laminin

poster abstractIntroduction: Streptococcus mutans, nicotine, and certain proteins may be involved in a complicated mechanism that contributes to atherosclerosis. Build up of arterial plaque causes atherosclerosis. Arterial plaque is mainly composed of fat, cholesterol, and calcium. When plaque builds up in the arteries, a clot or blockage can occur and may cause an occlusion. Objective: S. mutans grows in oral biofilm and causes dental caries. These bacteria enter the blood stream from mucosal breaks in the oral cavity. There is evidence that S. mutans binds to endothelial cell surface proteins lining arterial surfaces. An increased incidence of S. mutans in arterial plaque seems to have a direct relationship with atherosclerosis. From preliminary research, there was a strong indication that increased S. mutans biofilm formation is caused by nicotine. The number of binding proteins on nicotine-treated S. mutans cell surface increases as well. In addition, results demonstrated that S. mutans binds to collagen type I, fibrinogen, fibronectin, and laminin, which are proteins found on endothelial cells. Methods: To investigate protein binding, S. mutans UA159 was cultured in 0, 0.25, 0.50, 1.0, 2.0, and 4.0 mg/ml of nicotine and their ability to bind to human collagen type I, fibrinogen, fibronectin and laminin was assessed using an ELISA assay. Results: S. mutans significantly bound to collagen type I and fibrinogen when cultured in 2 and 4 mg/ml nicotine. S. mutans significantly bound to laminin when the bacterium was grown in 1, 2, and 4 mg/ml. The binding of S. mutans to fibronectin varied when cultured in different concentrations of nicotine. Conclusion: From the results, it can be concluded that S. mutans UA159 binds to collagen type I, fibrinogen, fibronectin, and laminin. This indicates that S. mutans and the proteins studied are very likely to be part of the mechanism that leads to atherosclerosis