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Chinese HPHT diamonds have improved dramatically in recent years. However, this brings a challenge in identifying type IIa colorless diamonds. In this study, eleven HPHT and three natural, colorless, gem-quality IIa diamonds were analyzed using magnified observation, Raman, PL and chemical element analysis. The results show that only HPHT samples possessed kite-like inclusions and lichenoid inclusions, as verified by their complex Raman spectra (100–750 cm−1). Through PL mapping, HPHT and natural IIa diamonds were distinguished by their growth environments, which were reflected by PL peaks at 503, 505, 575, 637, 693, 694 and 737 nm. The chemical components of HPHT IIa diamond carbide inclusions are mainly Fe, Co, Ni and Mn, but those of Natural IIa are mainly Fe and Ni. As a result, the chemical components can be used to distinguish a natural colorless IIa diamond from a synthetic diamond. [ABSTRACT FROM AUTHOR]

NFBD1, a signal amplifier of the p53 pathway, is vital for protecting cells from p53-mediated apoptosis and the early phase of DNA damage response under normal culture conditions. Here we investigated its expression in patients with nasopharyngeal carcinoma (NPC), and we describe the biological functions of the NFBD1 gene. We found that NFBD1 mRNA and protein were more highly expressed in NPC tissues than in nontumorous tissues. To investigate the function of NFBD1, we created NFBD1-depleted NPC cell lines that exhibited decreased cellular proliferation and colony formation, an increase in their rate of apoptosis, and an enhanced sensitivity to chemotherapeutic agents compared with in vitro controls. However, N -acetyl cysteine (NAC) and downregulation of p53 expression could partially reverse the apoptosis caused by the loss of NFBD1. Further analysis showed that loss of NFBD1 resulted in increased production of intracellular reactive oxygen species (ROS) depending on p53, which subsequently triggered the mitochondrial apoptotic pathway. Using a xenograft model in nude mice, we showed that silencing NFBD1 also significantly inhibited tumor growth and led to apoptosis. Taken together, our data suggest that inhibition of NFBD1 in NPC could be therapeutically useful. [ABSTRACT FROM AUTHOR]

Insufficient hydrogen peroxide content in tumor cells, unsuitable pH and low efficiency of commonly used metal catalysts severely affect the efficiency of chemodynamic therapy, resulting in unsatisfactory efficacy of chemodynamic therapy alone. For this purpose, we designed a composite nanoplatform capable of targeting tumors and selectively degrading in the tumor microenvironment (TME) to address these issues. In this work, we synthesized Au@Co 3 O 4 nanozyme inspired by crystal defect engineering. The addition of Au determines the formation of oxygen vacancies, accelerates electron transfer, and enhances redox activity, thus significantly enhancing the superoxide dismutase (SOD)-like and catalase (CAT)-like catalytic activities of the nanozyme. Subsequently, we camouflaged the nanozyme using a biomineralized CaCO 3 shell to avoid damage to normal tissues by the nanozyme while effectively encapsulating the photosensitizer IR820, and finally the tumor targeting ability of the nanoplatform was enhanced by the modification of hyaluronic acid. Under near-infrared (NIR) light irradiation, the Au@Co 3 O 4 @CaCO 3 /IR820@HA nanoplatform not only visualizes the treatment with multimodal imaging, but also plays a photothermal sensitizing role through various strategies, while enhancing the enzyme catalytic activity, cobalt ion-mediated chemodynamic therapy (CDT) and IR820-mediated photodynamic therapy (PDT), and achieving the synergistic enhancement of reactive oxygen species (ROS) generation. [ABSTRACT FROM AUTHOR]

Accurate diagnosis and precise and effective treatment are currently the two magic weapons for dealing with cancer. However, a single marker is often associated with multiple cellular events, which is not conducive to accurate diagnosis, and overly mild treatment methods often make the treatment effect unsatisfactory. In this paper, we construct a Au/Pd octopus nanoparticle-DNA nanomachine (Au/Pd ONP-DNA nanomachine) as a fully automatic diagnosis and treatment logic system. In this system, multiple DNA components are targeting detection units, Au/Pd ONPs act as carriers, and Au/Pd ONPs with an 808 nm laser is the treatment unit. In order to achieve the purpose of precise treatment, we will detect two secondary markers under the premise of detecting one major tumor marker. When all of the designated targets are detected (the logic system input is (1, 1, 1), and the output is (1, 1)), the 808 nm laser can be programmed to automatically radiate tumors and perform photothermal therapy and photodynamic therapy. In vivo and in vitro experiments show that this logic system not only can accurately identify tumor cells but also has considerable therapeutic effects.

NFBD1, a signal amplifier of the p53 pathway, is vital for protecting cells from p53-mediated apoptosis and the early phase of DNA damage response under normal culture conditions. Here we investigated its expression in patients with nasopharyngeal carcinoma (NPC), and we describe the biological functions of the NFBD1 gene. We found that NFBD1 mRNA and protein were more highly expressed in NPC tissues than in nontumorous tissues. To investigate the function of NFBD1, we created NFBD1-depleted NPC cell lines that exhibited decreased cellular proliferation and colony formation, an increase in their rate of apoptosis, and an enhanced sensitivity to chemotherapeutic agents compared with in vitro controls. However, N-acetyl cysteine (NAC) and downregulation of p53 expression could partially reverse the apoptosis caused by the loss of NFBD1. Further analysis showed that loss of NFBD1 resulted in increased production of intracellular reactive oxygen species (ROS) depending on p53, which subsequently triggered the mitochondrial apoptotic pathway. Using a xenograft model in nude mice, we showed that silencing NFBD1 also significantly inhibited tumor growth and led to apoptosis. Taken together, our data suggest that inhibition of NFBD1 in NPC could be therapeutically useful.