The antibacterial activity of photocatalytic titanium dioxide (TiO 2 ) substrates is induced primarily by UV light irradiation. Recently, nitrogen-and carbon-doped TiO 2 substrates were shown to exhibit photocatalytic activities under visible-light illumination. Their antibacterial activity, however, remains to be quantified. In this study, we demonstrated that nitrogen-doped TiO 2 substrates have superior visible-light-induced bactericidal activity against Escherichia coli compared to pure TiO 2 and carbon-doped TiO 2 substrates. We also found that protein-and light-absorbing contaminants partially reduce the bactericidal activity of nitrogen-doped TiO 2 substrates due to their light-shielding effects. In the pathogen-killing experiment, a significantly higher proportion of all tested pathogens, including Shigella flexneri, Listeria monocytogenes, Vibrio parahaemolyticus, Staphylococcus aureus, Streptococcus pyogenes, and Acinetobacter baumannii, were killed by visible-light-illuminated nitrogen-doped TiO 2 substrates than by pure TiO 2 substrates. These findings suggest that nitrogen-doped TiO 2 has potential application in the development of alternative disinfectants for environmental and medical usages.

More reliable biomarkers using near-patient technologies are needed to improve early diagnosis and intervention for patients with renal disease. Infrared (IR) vibrational spectroscopy/microspectroscopy is an established analytical method that was first used in biomedical research over 20 years ago. With the advances in instrumentation, computational and mathematical techniques, this technology has now been applied to a variety of diseases; however, applications in nephrology are just beginning to emerge. In the present study, we used attenuated total reflectance Fourier transform infrared (ATR-FTIR) spectroscopy to analyze urine samples collected from rodent models of inflammatory glomerulonephritis (GN) as well as from patients with crescentic GN, with the aim of identifying potential renal biomarkers; several characteristic mid-IR spectral markers were identified in urine samples. Specifically, a 1545 cm−1 band increased in intensity with the progression and severity of GN in rats, mice and humans. Furthermore, its intensity declined significantly in response to corticosteroid treatment in nephritic rats. In conclusion, our results suggest that specific urinary FTIR biomarkers may provide a rapid, sensitive and novel non-invasive means of diagnosing inflammatory forms of GN, and for real-time monitoring of progress, and response to treatment.

The prtV gene, encoding a collagenase of Vibrio parahaemolyticus, was expressed in Escherichia coli and purified by affinity chromatography. The transformant E. coli BL2l (DE3)(pPRT2) secreted the recombinant Prtv, and the highest enzyme activity was detected in the culture supernatant after 5 h IPTG induction. The molecular mass o f purified PrtV was 62 kDa as determined by gel filtration, which was similar to that obtained by SDS-PAGE (64 kDa). This suggested that PrtV was a monomer protein having no subunit structure. The isoelectric point o f PrtV was 852. In addition, PrtV contained a 27 amino acid signal peptide, and the amino acid composition of the PrtV showed satisfactory agreement with that predicted from the DNA sequence. The optimum temperature and pH of PrtV were 40 OC and pH 7.5, respectively. The activity of PrtV was inhibited by chelators such as EDTA, EGTA and 1,lOphenanthroline; however, its activity was restored by the addition of various metal ions (Co2+, Mn2+, Ca2+, Cu2+, Ni2+ and Zn2+), indicating that PrtV is a metalloprotease. PrtV degraded both type I collagen and synthetic substrate FALGPA well, showing that PrtV is indeed a collagenase.

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Phosphatidylinositol 3-kinase (PI3K) pathway is important for platelet activation. Recent studies showed that PI3K and oscillative calcium could cross talk to each other and positively regulate integrin alpha (IIb)beta3-mediated outside-in signaling. However, the mechanism of this feedback regulation remains to be further characterized. Here we found that treatments of both PI3K inhibitor wortmannin and P2Y1 inhibitor A3P5P could inhibit granular secretion in platelets. Additionally, when RGD-substrate adherent platelets were treated with the ADP scavenger apyrase to deplete the granular-released ADP, their attachments in engaging with substrates became looser and the frequency of calcium oscillation decreased. Since it is known that ADP stimulates the PI3K and calcium signal primarily through P2Y12 and P2Y1 receptors respectively, our data indicated that integrin alpha(IIb)beta3 downstream PI3K and calcium activation might be not completely coupled to integrin associated signaling complex, but in part through feedback stimulation by granular released ADP. Our data indicates the important roles of PI3K and granular released ADP in coordinating the feedback regulations in integrin alpha(IIb)beta3-mediated platelet activation.