The Safety and Anti-Tumor Effects of Ozonated Water in Vivo

Ozonated water is easier to handle than ozone gas. However, there have been no previous reports on the biological effects of ozonated water. We conducted a study on the safety of ozonated water and its anti-tumor effects using a tumor-bearing mouse model and normal controls. Local administration of ozonated water (208 mM) was not associated with any detrimental effects in normal tissues. On the other hand, local administration of ozonated water (20.8, 41.6, 104, or 208 mM) directly into the tumor tissue induced necrosis and inhibited proliferation of tumor cells. There was no significant difference in the number of terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick-end labeling (TUNEL)-positive cells following administration of ozonated water. The size of the necrotic areas was dependent on the concentration of ozonated water. These results indicate that ozonated water does not affect normal tissue and damages only the tumor tissue by selectively inducing necrosis. There is a possibility that it exerts through the production of reaction oxygen species (ROS). In addition, the induction of necrosis rather than apoptosis is very useful in tumor immunity. Based on these results, we believe that administration of ozonated water is a safe and potentially simple adjunct or alternative to existing antineoplastic treatments.     

A computational characterization of CO@C60

The carbon monoxide encapsulation into C₆₀ is evaluated using the DFT and MP2 calculations. The CO encapsulation is attractive, yielding an energy gain of more than 12 kcal/mol. This substantial encapsulation energy should produce at the conditions used in the high-temperature and high-pressure synthesis (originally used for encapsulation of rare gases in fullerenes) an equilibrium CO@C₆₀ fraction of about 3.5% compared to the empty C₆₀. The computed IR and NMR spectra agree with the available observations for CO encapsulated into open-cage C₆₀ derivatives.     

Identifying DNA methylation in a nanochannel

DNA methylation is a stable epigenetic modification, which is well known to be involved in gene expression regulation. In general, however, analyzing DNA methylation requires rather time consuming processes (24–96 h) via DNA replication and protein modification. Here we demonstrate a methodology to analyze DNA methylation at a single DNA molecule level without any protein modifications by measuring the contracted length and relaxation time of DNA within a nanochannel. Our methodology is based on the fact that methylation makes DNA molecules stiffer, resulting in a longer contracted length and a longer relaxation time (a slower contraction rate). The present methodology offers a promising way to identify DNA methylation without any protein modification at a single DNA molecule level within 2 h.     

Function of aluminum in crystal structure of rare earth–Mg–Ni hydrogen-absorbing alloy and deterioration mechanism of Nd0.9Mg0.1Ni3.5 and Nd0.9Mg0.1Ni3.3Al0.2 alloys

We investigated in detail the effect of incorporating Al in the crystal structure of rare earth–Mg–Ni hydrogen-absorbing alloys, which were developed as candidate materials for the metal hydride (MH) negative electrode in commercial Ni–MH batteries, using synchrotron powder X-ray diffraction. Partially substituting the Ni part with Al changes the lattice parameter of the major A₂B₇ phase, eliminating a mismatch between the AB₂ units and the AB₅ units. The change of the lattice parameter in the alloy leads to good hydrogen reversibility and good durability. Furthermore, we observed the alloy after 30 hydrogen absorption–desorption cycles using a scanning transmission electron microscope image. Consequently, we found that the surface layer of the Nd_0.9Mg_0.1Ni_3.5 alloy had an amorphous state, while the surface layer of the Nd_0.9Mg_0.1Ni_3.3Al_0.2 alloy did not. We confirmed that the deterioration mechanism of the Nd_0.9Mg_0.1Ni_3.3Al_0.2 alloy was due to partial expansion of the AB₂ unit along the c-axis; the local area of deterioration expanded during the cycling period.     

G Protein-Coupled Receptor 87 (GPR87) Promotes Cell Proliferation in Human Bladder Cancer Cells

G protein-coupled receptor 87 (GPR87) is a newly deorphanized member of the cell surface molecule G protein-coupled receptor family. GPR signaling was shown to play a role in promotion of cell growth and survival, metastasis, and drug resistance. The overexpression of GPR87 has also been reported in many malignant tumors including bladder cancer. The aim of the present study is to examine the effect of silencing GPR87 expression with a replication-deficient recombinant adenoviral vector expressing short hairpin RNA targeting GPR87 (Ad-shGPR87) and to explore the underlying molecular mechanisms in bladder cancer cells. Six GPR87-expressing human bladder cancer cells, HT1197, HT1376, J82, RT112, TCCSUP and UMUC3, were used. Infection with Ad-shGPR87 effectively downregulated the GPR87 expression, and significantly reduced the percentage of viable cells in 4 of 6 cell lines as detected by an MTT assay. Significant inhibition on cell proliferation with Ad-shGPR87 was observed in the wild-type p53 bladder cancer cell lines (HT1197, RT112, TCCSUP and UMUC3), but not in the mutant p53 cells (HT1376 and J82). As represented by a wild-type p53 RT112 cell, Ad-shGPR87 infection significantly enhanced p53 and p21 expression and caused caspase-dependent apoptosis. Furthermore, the treatment with Ad-shGPR87 exerted a significant antitumor effect against the GPR87-expressing RT112 xenografts. GPR87 appeared to be a promising target for gene therapy, and Ad-shGPR87 had strong antitumor effects, specifically anti-proliferative and pro-apoptotic effects, against GPR87-expressing human bladder cancer cells.     

Organochlorine contaminants in human adipose tissues from China: mass balance approach for estimating historical Chinese exposure to DDTs

Concentrations of persistent organochlorines (OCs), such as DDTs, hexachlorocyclohexanes (HCHs), hexachlorobenzene (HCB), polychlorinated biphenyls (PCBs), and chlordane compounds (CHLs) were determined in 34 human adipose tissues collected from Guizhou Province, southern China, during 2002. DDT was the predominant contaminant among OCs analyzed; concentrations ranged from 420 to 20 000 ng/g on a lipid wt basis (average +/- sd: 5700 +/- 4100 ng/g). Concentrations of DDTs and the ratio of p,p'-DDT/ sigmaDDT in humans in China were significantly higher than those reported for developed countries. DDT levels in humans in Guizhou Province were comparable to those from Shanghai City, implying the presence of significant sources of DDTs in inland and coastal areas in China. Age-dependent accumulation of HCH concentration was found in this study, possibly because of the considerable reduction in average dairy intake (ADI) of HCHs by Chinese during the recent two decades. On the basis of the information of the ADI rates, half-lives, and body burdens of DDTs, the magnitude of historical DDT exposures by Chinese was estimated. This suggested that approximately 80% of DDTs deposited in Chinese adipose tissues was accumulated before the 1990s. The monitoring of OC levels and epidemiological studies are needed in China to understand the status of contamination and the risks to humans.