The
proposed work involves the development of an autonomous, label-free
electrochemical sensor for real-time monitoring of cortisol levels
expressed naturally in sub-microliter sweat volumes, for prolonged
sensing periods of ∼8 h. Highly specific single-stranded DNA
(ssDNA) aptamer is used for affinity capture of cortisol hormone eluted
in sweat dynamically. The cortisol present in sweat binds to the aptamer
capture probe that changes conformation and modulates electrochemical
properties at the electrode–buffer interface, which was studied
using dynamic light scattering studies for the entire physiological
sweat pH. Attenuated total reflectance-Fourier transform infrared
spectroscopy and UV–vis spectroscopy were used to optimize
the binding chemistry of the elements of the sensor stack. Nonfaradaic
electrochemical impedance spectroscopy was used to calibrate the sensor
for a dynamic range of 1–256 ng/mL. An R
2 of 0.97 with an output signal range of 20–50% was
obtained. Dynamic cortisol level variation tracking was studied using
continuous dosing experiments to calibrate the sensor for temporal
variation. The sensor did not show significant susceptibility to noise
due to cross-reactive interferents and nonspecific buffer constituents.
The performance of the developed aptasensor was compared with the
previously established cortisol immunosensor in terms of surface charge
behavior and nonfaradaic biosensing. The aptamer sensor shows a higher
signal-to-noise ratio, better resolution, and has a larger output
range for the same input range as the cortisol immunosensor. The feasibility
of deploying the developed aptasensing scheme as continuous lifestyle
and performance monitors was validated through human subject studies.
Phenethyl isothiocyanate (PEITC), an effective anticancer and chemopreventive agent, has been reported to inhibit cancer cell growth through cell-cycle arrest and induction of apoptotic events in various human cancer cells models. However, whether PEITC inhibits human oral squamous cell carcinoma HSC-3 cell growth and its underlying mechanisms is still not well elucidated. In the present study, we evaluated the inhibitory effects of PEITC in HSC-3 cells and examined PEITC-modulated cell-cycle arrest and apoptosis. The contrast-phase and flow cytometric assays were used for examining cell morphological changes and viability, respectively. The changes of cell-cycle and apoptosis-associated protein levels were determined utilizing Western blotting in HSC-3 cells after exposure to PEITC. Our results indicated that PEITC effectively inhibited the HSC-3 cells' growth and caused apoptosis. PEITC induced G
0/G
1 phase arrest through the effects of associated protein such as p53, p21, p17, CDK2 and cyclin E, and it triggered apoptosis through promotion of Bax and Bid expression and reduction of Bcl-2, leading to decrease the levels of mitochondrial membrane potential (ΔΨm), and followed the releases of cytochrome c, AIF and Endo G then for causing apoptosis in HSC-3 cells. These results suggest that PEITC could be an antitumor compound for oral cancer therapy.
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