In recent years, efficient indoor organic photovoltaics (OPVs) have emerged as promising energy harvesters to drive Internet of Nanothings (IoNT) applications. The diverse design strategies developed for non-fullerene acceptor (NFA) materials have dramatically increased the power conversion efficiency (PCE) of indoor OPVs to 31%, and progress tends to continue. In this context, the current study investigated the indoor performance of NFA-OPVs by modifying the chalcogen-containing heterocycle of the acceptor molecule to thiophene (ThTh) and selenophene (ThSe), and changing the length of the external side chain using n-hexyl (C6) and n-nonyl (C9) components. Compared with the ThSe systems, the ThTh-containing OPVs exhibited enhanced current densities (JSC) and open-circuit voltages (VOC) owing to their enhanced crystallinity and reduced degree of bimolecular recombination. Similarly, the introduction of a short side chain (i.e., C6) led to relatively reduced monomolecular recombination and a moderated planarity compared to the system modified with the long side chain (i.e., C9). Ultimately, this resulted in an enhanced JSC and improved charge transport properties. Finally, the optimized OPV exhibited a PCE of 24.6% under a 1000 lx light-emitting diode lamp.
Abstract The tumor suppressor protein p16INK4a is a member of the INK4 family of cyclin-dependent kinase (Cdk) inhibitors, which are involved in the regulation of the eukaryotic cell cycle. However, the mechanisms underlying the anti-proliferative effects of p16INK4a have not been fully elucidated. Using yeast two-hybrid screening, we identified the eukaryotic elongation factor (eEF)1A2 as a novel interacting partner of p16INK4a. eEF1A2 is thought to function as an oncogene in cancers. The p16INK4a protein interacted with all but the D2 (250-327 aa) domain of eEF1A2. Computational docking study predicted that D24/D131 residues of p16INK4a interacted with eEF1A2 and it was confirmed by pull-down assay with mutant p16INK4a (D24A/D131E). Ectopic expression of p16INK4a decreased the expression of eEF1A2 and inhibited cancer cell growth. Furthermore, suppression of protein synthesis by expression of p16INK4a ex vivo was verified by luciferase reporter activity. Microinjection of p16INK4a mRNA into the cytoplasm of Xenopus embryos suppressed the luciferase mRNA translation, whereas the combination of p16INK4a and morpholino-eEF1A2 resulted in a further reduction in translational activity. We conclude that the interaction of p16INK4a with eEF1A2, and subsequent downregulation of the expression and function of eEF1A2 is a novel mechanism explaining the anti-proliferative effects of p16INK4a. Citation Format: Mee-Hyun Lee, Bu Young Choi, Yong-Yeon Cho, Myoung Ok Kim, Sung-Hyun Kim, Cheol-Jung Lee, Ji Hong Song, Ann M. Bode, Zigang Dong, Yong-Joon Surh. Direct down-regulation of eEF1A2 by Tumor suppressor p16INK4a inhibits cancer cell growth. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 2471. doi:10.1158/1538-7445.AM2014-2471
Due to the exponential increase in the development and utilization of rare earth oxide nanoparticles (REO NPs) in various fields, the possibility of exposure in humans by inhalation has increased. However, there are little information about hazards of REO NPs and its mechanisms of toxicity. In this study, we evaluated the acute pulmonary inflammation using 10 REO NPs (Dy2O3, Er2O3, Eu2O3, Gd2O3 La2O3, Nd2O3, Pr6O11, Sm2O3, Tb4O7, and Y2O3) and four well-known toxic particles (CuO, NiO, ZnO, and DQ12). Minimum three doses per NP were instilled into the lungs of female Wistar rats at surface area dose metric and lung inflammation was evaluated at 24 h post-instillation by bronchoalveolar lavage fluid (BALF) analysis and histopathological observation. All types of REO NPs showed common pathological changes including mild to moderate infiltration of neutrophils and activated macrophages in the alveoli, peribronchial, and perivascular region. The inflammogenic potential evaluated by the number of granulocytes divided by the treated surface area dose showed all types of REO NPs has much higher inflammogenic potential than DQ12, ZnO, and NiO NPs. The correlation plot between the number of granulocytes and the potential for reactive oxygen species (ROS) generation showed a good correlation with exception of Pr6O11. The higher inflammogenic potential of REO NPs than that of well-known highly toxic particles imply that REO NPs need special attention for inhalation exposure and more studies are needed. In addition, the potential of ROS generation is one of the key factors producing lung inflammation by REO NPs.
To evaluate the therapeutic activity and safety of paclitaxel and cisplatin combination chemotherapy in patients with advanced or metastatic gastric cancers that are unresponsive to primary chemotherapy.Advanced or metastatic gastric cancer patients unresponsive to first line chemotherapy were entered into this trial. The treatment regimen consisted of paclitaxel, 175 mg/m(2) by 3-hour infusion on day 1, and cisplatin, 60 mg/m(2) by 1 hour infusion on day 1, with the treatment repeated every 3 weeks.37 patients were entered in this study, with 32 fully evaluable for response. 4 (13%), 13 (40%) and 15 (47%) patients achieved a partial response, stable disease and progressed, respectively. The median time to progression was 4.0 months (95% CI: 2.0 approximately 6.0 months), and the median overall survival was 12.6 months (95% CI: 5.5 approximately 19.7 months), with a 1-year survival rate of 54%. Of a total of 135 cycles of chemotherapy, grades 3 and 4 hematological toxicities were neutropenia (14%) and anemia (3%). Grade >or=2 neuropathy was observed in 6 patients (17%).The combination of paclitaxel and cisplatin is an effective and tolerable salvage treatment modality for advanced gastric cancer.
Human skins are exposed to nanomaterials in everyday life from various sources such as nanomaterial-containing cosmetics, air pollutions, and industrial nanomaterials. Nanomaterials comprising metal haptens raises concerns about the skin sensitization to nanomaterials. In this study, we evaluated the skin sensitization of nanomaterials comparing metal haptens in vivo and in vitro . We selected five metal oxide NPs, containing copper oxide, cobalt monoxide, cobalt oxide, nickel oxide, or titanium oxide, and two types of metal chlorides (CoCl 2 and CuCl 2 ), to compare the skin sensitization abilities between NPs and the constituent metals. The materials were applied to KeratinoSens TM cells for imitated skin-environment setting, and luciferase induction and cytotoxicity were evaluated at 48 h post-incubation. In addition, the response of metal oxide NPs was confirmed in lymph node of BALB/C mice via an in vivo method. The results showed that CuO and CoO NPs induce a similar pattern of positive luciferase induction and cytotoxicity compared to the respective metal chlorides; Co 3 O 4 , NiO, and TiO 2 induced no such response. Collectively, the results implied fast-dissolving metal oxide (CuO and CoO) NPs release their metal ion, inducing skin sensitization. However, further investigations are required to elucidate the mechanism underlying NP-induced skin sensitization. Based on ion chelation data, metal ion release was confirmed as the major “factor” for skin sensitization.
장기종은 소화기 장벽내 공기가 축적되는 방사선학적 소견이다. 장기종의 원인은 매우 다양하여 그 원인이 아직 명확하지 않다. 백혈병 환자에서 장기종은 약물치료 및 수술적 치료가 필요한 드문 합병증이다. 대부분의 장기종은 경과 및 예후가 좋은 편이지만 응급수술이 필요한 경우도 있으므로 치료 결정이 어려울 때가 많다. 저자들은 불응성 급성전구B 림프모세포백혈병 환자에서 백혈병의 진행과정으로서 장기종이 발생하여 결국 패혈증으로 사망한 증례를 경험하여 보고하는 바이다.
Purpose To determine the activity and toxicities of low dose leucovorin (LV) plus fluorouracil (5-FU) regimen, combined with oxaliplatin every two weeks (modified FOLFOX 4), as a first-line therapy for patients with metastatic colorectal cancer. Materials and Methods Between March 2001 and August 2003, fifty-five patients were enrolled in this study. Patients were treated with oxaliplatin 85 mg/m2 as a 2-hour infusion at days 1 plus LV 20 mg/m2 over 10 minutes, followed by 5-FU bolusa 400 mg/m2 bolus and 22 hour continuous infusion of 600 mg/m2 5-FU at day 1~2. This treatment was repeated in 2 week intervals. Results The objective response rate was 40% on an intent-to-treatment analysis. Three patients (6%) demonstrated a complete response and nineteen patients (38%) showeda partial response. Sixteen patients (32%) showed a stable disease and eleven patients (22%) progressed during the course of the treatment. The median time to progression and overall survival time wereas 6.6 months (95% CI: 4.98~8.02 months) and the median overall survival time was 17.0 months (95% CI: 9.15~24.85 months) from the start of the chemotherapy, respectively. A total of 275 cycles were analyzed for toxicity. Major hematologic toxicities included grade 1~2 anemia (23.5%), neutropenia (25.3%) and thrombocytopenia (10.6%). There were only 2 cycles of neutropenic fever. The most common non-hematologic toxicities were grade 1~2 nausea/vomiting (10.9%), diarrhea (9.1%) and grade 1 neuropathy (18.0%). There was no treatment related death. Conclusion The modified folfox 4 regimen is safe and effective regimen as a first-line therapy in advanced colorectal cancer patients. Key words: Colorectal neoplasm, Chemotherapy, Oxaliplatin, 5-FU, Leucovorin
Waldenstrom macroglobulinemia, which is characterized by elevation of serum monoclonal IgM paraprotein, has recently been responsible for the treatment of purine analogues. Fludarabine, one of purine analogues, has been associated with autoimmune hemolytic anemia in patient with chronic lymphocytic leukemia. However, autoimmune hemolytic anemia after fludarabine treatment for Waldenstrom macroglobulinemia has not been reported. We experienced a case of autoimmune hemolytic anemia after fludarabine treatment for Waldenstrom macroglobulinemia. In this case, hemolytic anemia with positive direct Coombs' test occurred at 20 months after the first administration of fludarabine, relapsed at 5 days after re-administration. This anemia responded to steroid therapy. Autoimmune hemolytic anemia associated with fludarabine therapy can be severe and fatal, especially if a patient is re-treated with this drug after a previous episode of hemolytic anemia.
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