Background
211At is a high-energy α-ray emitter with a relatively short half-life and a high cytotoxicity for cancer cells. Its dispersion can be imaged using clinical scanners, and it can be produced in cyclotrons without the use of nuclear fuel material. This study investigated the biodistribution and the antitumor effect of 211At-labeled gold nanoparticles (211At-AuNP) administered intratumorally.
Results
AuNP with a diameter of 5, 13, 30, or 120 nm that had been modified with poly (ethylene glycol) methyl ether (mPEG) thiol and labeled with 211At (211At-AuNP-S-mPEG) were incubated with tumor cells, or intratumorally administered to C6 glioma or PANC-1 pancreatic cancers subcutaneously transplanted into rodent models. Systemic and intratumoral distributions of the particles in the rodents were then evaluated using scintigraphy and autoradiography, and the changes in tumor volumes were followed for about 40 days. 211At-AuNP-S-mPEG was cytotoxic when it was internalized by the tumor cells. After intratumoral administration, 211At-AuNP-S-mPEG became localized in the tumor and did not spread to systemic organs during a time period equivalent to 6 half-lives of 211At. Tumor growth was strongly suppressed for both C6 and PANC-1 by 211At-AuNP-S-mPEG. In the C6 glioma model, the strongest antitumor effect was observed in the group treated with 211At-AuNP-S-mPEG with a diameter of 5 nm.
Conclusions
The intratumoral single administration of a simple nanoparticle, 211At-AuNP-S-mPEG, was shown to suppress the growth of tumor tissue strongly in a particle size-dependent manner without radiation exposure to other organs caused by systemic spread of the radionuclide.
Graphic Abstract
The broadband spectroscopic analysis over Brillouin, quasi-elastic, and Raman regions arising from the same position of the sample has been achieved by employing an ultra-narrowband holographic notch filter (HNF) and an optical isolator. Recently, HNFs are often employed to reject strong elastic scattering in low-frequency Raman experiments. Meanwhile, the rejected spectral component agrees with the frequency range that can be observed by a triple-pass tandem Fabry–Pérot interferometer. Thus the broadband spectroscopy can be accomplished by introducing the rejected light to the interferometer. This system, in combination with the local symmetry analysis by polarization-direction-resolved Raman spectroscopy, is particularly advantageous for the investigation of spatially inhomogeneous systems.
The effect of bovine -casein (1-28) purified from commercial casein phosphopeptide preparations on human T, B, and monocyte cell lines was evaluated. Beta-casein (1-28) enhanced the proliferation of the following: T cell lines HUT-78, Jurkat Clone E6-1, and MOLT-4; B cell lines BALL, KHM-1B, and U266B1; and monocyte cell lines U937 and HL-60. Moreover, -casein (1-28) stimulated IgA production by KHM-1B over 96 h of culture. Semiquantitative reverse transcriptional-polymerase chain reaction analysis indicated that -casein (1-28) enhanced mRNA expression of interleukin (IL)-6 in U266B1 and KHM-1B. These results suggest that -casein (1-28) exerts a mitogenic effect on human T, B, and monocyte cells, and an IgA-enhancing effect on B cells.
We evaluated density and chemical bonding states of the CVD SiO2 film with and without plasma treatment to clarify an effect of the plasma treatment. It was found that the chemical bonding states were homogenized by the plasma treatment from the results of X-ray photoelectron spectroscopy. In addition, an increase of the film density was also observed. These results indicate the densification of SiO2 film, suppression of bond-angle fluctuation, and decrease of impurities (e.g. Hydrogen, Nitrogen and so on) in the SiO2 film. These results can well explain the improvement of the electrical properties by the plasma treatment. Furthermore, UV-Raman measurement was performed to evaluate the modification of Si stress and crystal quality at the SiO2/Si interface.
Pulmonary tumor thrombotic microangiopathy (PTTM) is a fatal malignancy-related condition that involves rapidly progressing hypoxia and pulmonary hypertension. We report a case of PTTM caused by prostate carcinoma, which was diagnosed before autopsy in an 81-year-old man. Computed tomography showed diffuse ground-glass opacities, consolidation, and small nodules in the peripheral regions of the lung. Autopsy showed adenocarcinoma cells embolizing small pulmonary arteries with fibrocellular intimal proliferation, which was consistent with PTTM caused by prostate carcinoma.
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