The Effect of Antibacterial Agents Triclosan and N-alkyl on E. coli Viability

Within a society concerned with the spread of infectious disease, many common cleaning products boast high germ mortality rates. Consumers have learned to trust marketed disinfectants to protect them from disease causing microbes. While antibacterial\u27\u27 sells in the consumer pursuit of cleanliness, concerns regarding the overuse of antibacterial agents have recently arisen. Bacteria have the ability to mutate and become resistant to antibiotics. Resistant mutations can result from prolonged or repeated exposure of the bacteria to the antibiotic. Theoretically, the genes that code for resistance negatively affect the bacteria\u27s fitness. It is expected that a change in a gene\u27s normal function will alter the fitness of an organism. Therefore, when no longer exposed to the antibiotic, the bacteria may evolve backward and lose resistance in order to be a better competitor. But recent studies indicate that this is often not the case.1 The bacterium E.coli demonstrates reduced mutation reversion, and in many cases the development of further compensatory mutations in the absence of antibiotics. When consumers reach to antibacterial products to kill bacteria, they may actually be encouraging its growth. Creating a bacteria-free home may be futile, or even counterproductive

Comparison of Antibodies to Detect Uroplakin in Urothelial Carcinomas

Immunohistochemistry for Uroplakin (UP) II and III is used to determine urothelial origin of carcinomas of unknown primary site and are especially valuable to differentiate urothelial carcinomas (UCs) from lung squamous cell carcinomas and prostate carcinomas. In the Nordic immunohistochemical Quality Control assessment scheme, only 45% of the participants obtained a sufficient staining result for UP. Primary antibodies (Abs) against UPII were most successful with a pass rate of 86%. No Abs against UPIII provided sufficient staining results. A comparative study was carried out on a larger cohort of tissue samples with optimized methods for the UPII mouse monoclonal antibody (mmAb) clone BC21, UPIII mmAb clone AU-1, and rabbit monoclonal antibody (rmAb) clone SP73 to evaluate the performance in a standardized way. Tissue microarrays containing 58 UCs, 111 non-UCs, and 20 normal tissues were included. The UP stains were evaluated by using H-score. Based on H-scores, samples were categorized as high-expressor (150 to 300), moderate-expressor (10 to 149), low-expressor (1 to 9), and negative (150 for the UPII Ab. The 2 UPIII Abs gave an analytical specificity of 100% compared with 97% for the UPII Ab being positive in 2 ovarian carcinomas and 1 cervical squamous cell carcinoma

Parity detection and entanglement with a Mach-Zehnder interferometer

A parity meter projects the state of two qubits onto two subspaces with different parities, the states in each parity class being indistinguishable. It has application in quantum information for its entanglement properties. In our work we consider the electronic Mach-Zehnder interferometer (MZI) coupled capacitively to two double quantum dots (DQDs), one on each arm of the MZI. These charge qubits couple linearly to the charge in the arms of the MZI. A key advantage of an MZI is that the qubits are well separated in distance so that mutual interaction between them is avoided. Assuming equal coupling between both DQDs and the arms and the same bias for each DQD, this setup usually detects three different currents, one for the odd states and two for each even state. Controlling the magnetic flux of the MZI, we can operate the MZI as a parity meter: only two currents are measured at the output, one for each parity class. In this configuration, the MZI acts as an ideal detector, its Heisenberg efficiency being maximal. For a class of initial states, the initially unentangled DQDs become entangled through the parity measurement process with probability one.Comment: 9 pages, 2 figure

Identification of a residue in hepatitis C virus E2 glycoprotein that determines scavenger receptor BI and CD81 receptor dependency and sensitivity to neutralizing antibodies.

Hepatitis C virus (HCV) infection is dependent on at least three coreceptors: CD81, scavenger receptor BI (SR-BI), and claudin-1. The mechanism of how these molecules coordinate HCV entry is unknown. In this study we demonstrate that a cell culture-adapted JFH-1 mutant, with an amino acid change in E2 at position 451 (G451R), has a reduced dependency on SR-BI. This altered receptor dependency is accompanied by an increased sensitivity to neutralization by soluble CD81 and enhanced binding of recombinant E2 to cell surface-expressed and soluble CD81. Fractionation of HCV by density gradient centrifugation allows the analysis of particle-lipoprotein associations. The cell culture-adapted mutation alters the relationship between particle density and infectivity, with the peak infectivity occurring at higher density than the parental virus. No association was observed between particle density and SR-BI or CD81 coreceptor dependence. JFH-1 G451R is highly sensitive to neutralization by gp-specific antibodies, suggesting increased epitope exposure at the virion surface. Finally, an association was observed between JFH-1 particle density and sensitivity to neutralizing antibodies (NAbs), suggesting that lipoprotein association reduces the sensitivity of particles to NAbs. In summary, mutation of E2 at position 451 alters the relationship between particle density and infectivity, disrupts coreceptor dependence, and increases virion sensitivity to receptor mimics and NAbs. Our data suggest that a balanced interplay between HCV particles, lipoprotein components, and viral receptors allows the evasion of host immune responses