Extended Stern Model

In this paper, a theoretical approach of extended Stern model is formulated to represent the electric double layer (EDL) for biochemical as well as biological samples. The existing Stern model is used for several decades to describe the phenomena of electric double layer of electrode/electrolyte interface. In the conventional stern model the double layer which is formed between the electrode and electrolyte interface is described by double layer capacitance. Using the existing Stern model, the equivalent circuit model is not valid for electrical double layer capacitance of electrode/electrolyte interface in β dispersion range. The protein molecules form chemical coupling and chemical adsorption along with classical ionic bonding with gold electrodes. Thus, the compactness of EDL decreases and the double layer capacitance is replaced by a constant phase element (CPE). In the present paper, a three-electrode based ECIS device was used to measure the impedance of various enzymatic solutions for practical realization of theoretical approach. The results obtained from experimental work, were simulated by equivalent circuit simulator, ZsimpWin to validate the extended Stern model by comparing χ2 value. Finally the electrical parameters were extracted and compared for Stern model and extended Stern model. The results obtained by practical experiment and equivalent circuit simulation showed the effectiveness of extended Stern model over Stern model

A survey of chiral hypervalent iodine reagents in asymmetric synthesis

The recent years have witnessed a remarkable growth in the area of chiral hypervalent iodine chemistry. These environmentally friendly, mild and economic reagents have been used in catalytic or stoichiometric amounts as an alternative to transition metals for delivering enantioenriched molecules. Varieties of different chiral reagents and their use for demanding asymmetric transformations have been documented over the last 25 years. This review highlights the contribution of different chiral hypervalent iodine reagents in diverse asymmetric conversions

Monitoring cellular activities of cancer cells using impedance sensing devices

The present work reports the impedimetric characterization of cellular activities of T47D cells treated with anticancer drug ZD6474 using impedance sensing devices. Four types of devices with different dimensions are fabricated by micromachining technology. Real time impedance monitoring data reveals spreading stage completes within 5 h. The frequency response characteristics of drug treated cells are studied to evaluate cytotoxic effect of ZD6474 along with the sensitivity variation for different designs. Compared to control data, a significant decrease in impedance data is observed for drug treated samples above 10 μM dose due to predominant cell death and detachment from the electrode surfaces. The quantitative relation developed between cell impedance and drug dose indicates that the magnitude of cell impedance varies inversely with the drug dose

Assessing cytotoxic effect of ZD6474 on MDA-MB-468 cells using cell-based sensor

This paper presents the application of an impedance-based measurement of cytotoxicity of ZD6474 on MDA-MB-468 breast cancer cells in culture. In the present experiment, four types of cell-based sensors with different electrode geometries are fabricated by using microfabrication technology. MDA-MB-468 cells are grown on the electrode surfaces to study cell adhesion, spreading, and apoptosis. The real time impedance monitoring data show that the cells took to complete the spreading process on electrode surfaces. The cytotoxic effect of ZD6474 is dose dependant and with the increases of drug doses, the impedance value decreases, which correlates that ZD6474 blocks cell proliferation and induces apoptosis in breast cancer cells. A quantitative relationship, developed between the impedance and drug doses, establishes a negative correlation between the drug doses and impedance. General consistency has been found between the impedance response and the biochemical assay. Thus, impedance sensing method provides a simple and cost effective method to study chemical cytotoxicity in vitro

Acetylation of the proto-oncogene EVI1 abrogates Bcl-xL promoter binding and induces apoptosis.

EVI1 (Ecotropic Viral Integration site I), which was originally identified as a myeloid transforming gene by means of retroviral insertional mutagenesis in mouse leukemia, encodes a nuclear DNA binding zinc finger protein. The presence of zinc fingers that are able to bind to specific sequences of DNA suggests that EVI1 is a transcriptional regulator; however, except a few, target genes of EVI1 are poorly functionally identified thus far. In this study we provide evidence that EVI1 directly induces the expression of Bcl-xL through the first set of zinc finger and thereby inhibits apoptosis. ChIP analysis showed that EVI1 binds to the Bcl-xL promoter in HT-29 cells, a colon carcinoma cell line, which expresses EVI1. The observation is also supported by the fact that EVI1 siRNA treated HT-29 cells, shows a down regulation of Bcl-xL expression and that over expression of EVI1 results in the induction of the Bcl-xL reporter construct. A set of EVI1 positive chronic myeloid leukemia (CML) samples also showed higher Bcl-xL expression with respect to EVI1 negative samples. Interestingly, co-expression of EVI1 with wild type, but not with dominant-negative form of PCAF, abolishes the effect of EVI1 on Bcl-xL, indicating that acetylation of EVI1 abrogates its ability not only to bind Bcl-xL promoter but also alleviate Bcl-xL activity. Finally we have shown that EVI1 expression regulates apoptosis in HT-29 cells, which is abrogated when HT-29 cells are transfected with EVI1 siRNA or PCAF. The result for the first time shows a direct pathway by which EVI1 can protect cells from apoptosis and also demonstrates that the pathway can be reversed when EVI1 is acetylated

Electric cell–substrate impedance sensing technique to monitor cellular behaviours of cancer cells

The present work reports the cellular electrical behaviour of the MDA-MB-231 breast cancer cell line treated with the anticancer drug ZD6474, using impedance sensing devices. Microelectrode-based devices with four different electrode geometries are fabricated by microfabrication technology. Real-time impedance monitoring data show high impedance variation during the initial 5 hours, revealing rapid spreading of cells over electrode surfaces. It is further established that impedance variation is mostly controlled by cells covering the electrode surface area, and thus, an enhanced effect is seen with electrode devices with a smaller geometry. Real-time impedimetric cytotoxicity data reveal that cell death and detachment starts at 21 h after inoculation of cells in the devices. The frequency response characteristics of drug-treated cells are studied to evaluate the cytotoxic effect of ZD6474. Compared to the control, a significant variation in the magnitude of the measured impedance data is observed for drug-treated samples above a 5 μM dose, indicating cell growth suppression and cell death. Finally, an empirical relationship between cell impedance and drug dose is established from impedance data, which shows that they are negatively correlated

Frequency dependent impedimetric cytotoxic evaluation of anticancer drug on breast cancer cell

The present work reports the impedance characteristics of MCF-7 cell lines treated with anticancer drug ZD6474 to evaluate the cytotoxic effect on cellular electrical behaviour using miniature impedance sensors. Four types of impedance sensing devices with different electrode geometries are fabricated by microfabrication technology. The frequency response characteristics of drug treated cells are studied to evaluate cytotoxic effect of ZD6474 and also to assess the frequency dependent sensitivity variation with electrode area. A significant variation in magnitude of measured impedance data is obtained for drug treated samples above 10 μM dose indicating prominent effect of ZD6474 which results in suppression of cell proliferation and induction of apoptosis process. The results obtained by impedimetric method are correlated well with conventional in vitro assays such as flow cytometry, cell viability assays and microscopic imaging. Finally an empirical relation between cell impedance, electrode area and drug dose is established from impedance data which exhibits a negative correlation between drug doses and impedance of cancer cells