Adult T-cell Leukemia/Lymphoma (ATL) in the Nasal and Paranasal Cavity: Four Cases Report.

Adult T-cell leukemia/lymphoma (ATL) is a form of leukemia caused by the human T-cell leukemia virus type I (HTLV-1). Otolaryngologists often diagnose ATL based on cervical lymphadenopathy or Waldeyer ring lesions. However, there are few reports of ATL occurring in the nasal and paranasal cavity. Here, we report four such cases of ATL. Case 1: An 82-year-old man diagnosed with acute-type ATL with a tumor in the nasal cavity underwent 5 courses of THP-COP, but died after 36 months due to ATL. Case 2: A 62-year-old woman diagnosed with lymphoma-type ATL with a tumor in the frontal sinus was treated with 5 courses of VCAP-AMP-VECP, and has survived for more than 10 years. Case 3: A 64-year-old man diagnosed with lymphoma-type ATL with a tumor in the maxillary sinus underwent 8 courses of VCAP-AMP-VECP and 2 courses of mogamulizumab, but died after 34 months due to ATL. Case 4: A 52-year-old woman diagnosed with lymphoma-type ATL with tumors in both ethmoid sinuses received 2 courses of CHOP, 2 courses of DeVIC, radiotherapy (32 Gy) and 2 courses of mogamulizumab, but died after 9 months due to ATL.

Characterization of Influenza A(H1N1)pdm09 Viruses Isolated in the 2018-2019 and 2019-2020 Influenza Seasons in Japan.

The influenza A(H1N1)pdm09 virus that emerged in 2009 causes seasonal epidemic worldwide. The virus acquired several amino acid substitutions that were responsible for antigenic drift until the 2018-2019 influenza season. Viruses possessing mutations in the NA and PA proteins that cause reduced susceptibility to NA inhibitors and baloxavir marboxil, respectively, have been detected after antiviral treatment, albeit infrequently. Here, we analyzed HA, NA, and PA sequences derived from A(H1N1)pdm09 viruses that were isolated during the 2018-2019 and 2019-2020 influenza seasons in Japan. We found that A(H1N1)pdm09 viruses possessing the D187A and Q189E substitutions in HA emerged and dominated during the 2019-2020 season; these substitutions in the antigenic site Sb, a high potency neutralizing antibody-eliciting site for humans, changed the antigenicity of A(H1N1)pdm09 viruses. Furthermore, we found that isolates possessing the N156K substitution, which was predicted to affect the antigenicity of A(H1N1)pdm09 virus at the laboratory level, were detected at a frequency of 1.0% in the 2018-2019 season but 10.1% in the 2019-2020 season. These findings indicate that two kinds of antigenically drifted viruses-N156K and D187A/Q189E viruses-co-circulated during the 2019-2020 influenza season in Japan.

Improving the Open-Circuit Voltage of Sn-Based Perovskite Solar Cells by Band Alignment at the Electron Transport Layer/Perovskite Layer Interface.

Organic-inorganic lead halide perovskites are promising materials for realization of low-cost and high-efficiency solar cells. Because of the toxicity of lead, Sn-based perovskite materials have been developed as alternatives to enable fabrication of Pb-free perovskite solar cells. However, the solar cell performance of Sn-based perovskite solar cells (Sn-PSCs) remains poor because of their large open-circuit voltage (VOC) loss. Sn-based perovskite materials have lower electron affinities than Pb-based perovskite materials, which result in larger conduction band offset (CBO) values at the interface between the Sn-based perovskite and a conventional electron transport layer (ETL) material such as TiO2. Herein, the relationship between the VOC and the CBO in these devices was studied to improve the solar cell performances of Sn-PSCs. It was found that the band offset at the ETL/perovskite layer interface affects the VOC of the Sn-PSCs significantly but does not affect that of the Pb-PSCs because the Sn-based perovskite material is a p-type semiconductor, unlike the Pb-based perovskite. It was also found that Nb2O5 has the CBO that is closest to zero for Sn-based perovskite materials, and the VOC values of Sn-PSCs that use Nb2O5 as their ETL are higher than those of Sn-PSCs using TiO2 or SnO2 ETLs. This study indicates that control of the energy alignment at the ETL/perovskite layer interface is an important factor in improving the VOC values of Sn-PSCs.

Synthesis of ultrasmall Li-Mn spinel oxides exhibiting unusual ion exchange, electrochemical, and catalytic properties.

The efficient surface reaction and rapid ion diffusion of nanocrystalline metal oxides have prompted considerable research interest for the development of high functional materials. Herein, we present a novel low-temperature method to synthesize ultrasmall nanocrystalline spinel oxides by controlling the hydration of coexisting metal cations in an organic solvent. This method selectively led to Li-Mn spinel oxides by tuning the hydration of Li(+) ions under mild reaction conditions (i.e., low temperature and short reaction time). These particles exhibited an ultrasmall crystallite size of 2.3 nm and a large specific surface area of 371 ± 15 m(2) g(-1). They exhibited unique properties such as unusual topotactic Li(+)/H(+) ion exchange, high-rate discharge ability, and high catalytic performance for several aerobic oxidation reactions, by creating surface phenomena throughout the particles. These properties differed significantly from those of Li-Mn spinel oxides obtained by conventional solid-state methods.

Oxidative nucleophilic strategy for synthesis of thiocyanates and trifluoromethyl sulfides from thiols.

Thiocyanates and trifluoromethyl sulfides are important compounds and have classically been synthesized via multistep procedures together with the formation of significant amounts of byproducts. Herein, we demonstrate an oxidative nucleophilic strategy for the synthesis of thiocyanates and trifluoromethyl sulfides from thiol starting materials using nucleophilic reagents such as TMSCN and TMSCF3 (TMS = trimethylsilyl). In the presence of a 2 × 2 manganese oxide-based octahedral molecular sieve (OMS-2) and potassium fluoride (KF), various structurally diverse thiocyanates and trifluoromethyl sulfides could be synthesized in almost quantitative yields (typically >90%). The presented cyanation and trifluoromethylation reactions proceed through the OMS-2-catalyzed oxidative homocoupling of thiols to give disulfides followed by nucleophilic bond cleavage to produce the desired compounds and thiolate species (herein S-trimethylsilylated thiols). OMS-2 can catalyze oxidative homocoupling of the thiolate species, thus resulting formally in the quantitative production of thiocyanates and trifluoromethyl sulfides from thiols.

Fucoidan induces apoptosis through activation of caspase-8 on human breast cancer MCF-7 cells.

Fucoidan is an active component of seaweed that has been shown to inhibit proliferation and induce apoptotic cell death in several tumor cells. However, the detailed mechanisms underlying this process have not yet been elucidated. In the present report, we investigated the effect of fucoidan on the induction of apoptosis in human breast cancer MCF-7 cells. Our data demonstrated that fucoidan reduced the viable cell number of MCF-7 cells in a dose- and time-dependent manner. In contrast, fucoidan did not affect the viable cell number of normal human mammary epithelial cells. Results from the apoptosis assay demonstrated that fucoidan induced internucleosomal DNA fragmentation, chromatin condensation, activation of caspase-7, -8, and -9, and cleavage of poly(ADP ribose) polymerase. Furthermore, expression of Bid was decreased, whereas truncated Bid was increased by fucoidan treatment. There was also a decline in cytosolic Bax and a striking increase of cytosolic cytochrome c. Caspase-8-specific inhibitor, z-ITED-fmk, canceled the cytotoxicity of fucoidan, activation of caspase-7, -8, and -9, and a series of changes in Bax, Bid, and cytochrome c. However, caspase-9-specific inhibitor exerted a moderate inhibitory effect on the cytotoxicity of fucoidan. These data indicated that fucoidan could induce apoptotic cell death through a caspase-8-dependent pathway in MCF-7 cells.

Trans10, cis12-conjugated linoleic acid induces mitochondria-related apoptosis and lysosomal destabilization in rat hepatoma cells.

Conjugated linoleic acid (CLA) is a powerful anti-carcinogenic fatty acid. Previously, we showed that 10trans 12cis (10t, 12c) CLA induced apoptotic cell death in rat hepatoma. Here, we demonstrated significant cytotoxic effects of 1 muM 10t, 12c-CLA, but not 9c, 11t-CLA, on dRLh-84 rat hepatoma cells. 9t, 11t and 9c, 11c-CLA also showed low levels of cytotoxic activity. 10t, 12c-CLA activated caspase-3, 9 followed by cytochrome c release from mitochondria into the cytosol. Inhibitors of caspase-3, 9 blocked the cytotoxicity of 10t, 12c-CLA. 10t, 12c-CLA also induced translocation of Bax protein into the mitochondrial membrane and cleavage of Bid protein. Lysosomal destabilization induced by 10t, 12c-CLA was observed by monitoring the re-localization of Acridine Orange and the leakage of beta-hexosaminidase from lysosomes. 10t, 12c-CLA directly degraded the isolated lysosomes from the rat liver. Our observations indicate that 10t, 12c-CLA induces mitochondria-related apoptosis accompanied by lysosomal destabilization in rat hepatoma cells.