Raman Spectroscopy for Urea Breath Test.

The urea breath test is a non-invasive diagnostic method for Helicobacter pylori infections, which relies on the change in the proportion of 13CO2 in exhaled air. Nondispersive infrared sensors are commonly used for the urea breath test in laboratory equipment, but Raman spectroscopy demonstrated potential for more accurate measurements. The accuracy of the Helicobacter pylori detection via the urea breath test using 13CO2 as a biomarker is affected by measurement errors, including equipment error and δ13C measurement uncertainty. We present a Raman scattering-based gas analyzer capable of δ13C measurements in exhaled air. The technical details of the various measurement conditions have been discussed. Standard gas samples were measured. 12CO2 and 13CO2 calibration coefficients were determined. The Raman spectrum of the exhaled air was measured and the δ13C change (in the process of the urea breath test) was calculated. The total error measured was 6% and does not exceed the limit of 10% that was analytically calculated.

Detection of A and B Influenza Viruses by Surface-Enhanced Raman Scattering Spectroscopy and Machine Learning.

We demonstrate the possibility of applying surface-enhanced Raman spectroscopy (SERS) combined with machine learning technology to detect and differentiate influenza type A and B viruses in a buffer environment. The SERS spectra of the influenza viruses do not possess specific peaks that allow for their straight classification and detection. Machine learning technologies (particularly, the support vector machine method) enabled the differentiation of samples containing influenza A and B viruses using SERS with an accuracy of 93% at a concentration of 200 µg/mL. The minimum detectable concentration of the virus in the sample using the proposed approach was ~0.05 µg/mL of protein (according to the Lowry protein assay), and the detection accuracy of a sample with this pathogen concentration was 84%.

Apoptin enhances the oncolytic properties of vaccinia virus and modifies mechanisms of tumor regression.

A recombinant vaccinia virus VVdGF-ApoS24/2 expressing apoptin selectively kills human cancer cells in vitro [Kochneva et al., 2013]. We compared the oncolytic activity of this recombinant with that of the parental strain L-IVP using a model of human A431 carcinoma xenografts in nude mice. Single intratumoral injections (2×10^7 PFU/mouse) of the viruses produced a dramatic decrease in tumor volumes, which was higher after injection of apoptin-producing virus. The tumor dried out after the injection of recombinant while injection of L-IVP strain resulted in formation of cavities filled with cell debris and liquid. Both viruses rapidly spread in xenografts and replicate exclusively in tumor cells causing their destruction within 8 days. Both viruses induced insignificant level of apoptosis in tumors. Unlike the previously described nuclear localization of apoptin in cancer cells the apoptin produced by recombinant virus was localized to the cytoplasm. The apoptin did not induce a typical apoptosis, but it rather influenced pathway of cell death and thereby caused tumor shrinkage. The replacement of destroyed cells by filamentous material is the main feature of tumor regression caused by the VVdGF-ApoS24/2 virus. The study points the presence of complicated mechanisms of apoptin effects at the background of vaccinia virus replication.