Enhanced visible-light photocatalytic activity of anatase-rutile mixed-phase nano-size powder given by high-temperature heat treatment

Nano-size EVONIK AEROXIDE® P25 titanium dioxide, TiO2, powder was heat-treated at temperatures, 700–900°C, in air. An X-ray diffraction study showed that the P25 powder is composed of approximately 20 and approximately 80 mass% of rutile and anatase phases, respectively. It was also shown that the transformation from anatase to rutile induced by hightemperature heat treatment was almost completed at 750°C, whereas a small amount (less than 3 mass%) of anatase phase was still left even in the powder heat-treated at 900°C. The transformation behaviour was consistent with results obtained by Raman scattering spectroscopy. Raman experiments also indicated that high-temperature heating induced the formation of oxide ion vacancies. Powders were dispersed in methyl orange (MO) aqueous solution, and the bleach rate of MO was measured to evaluate photocatalytic activity under ultraviolet (UV)- and visible-light irradiation. After the heat treatment, the UV-light photocatalytic performance sharply deteriorated. Interestingly, visible-light photocatalytic activity was enhanced by high-temperature heating and reached the highest performance for an 800°C-heated sample, indicating that the P25 powder obtained high visible-light photocatalytic performance after heat treatment. Even after 900°C heat treatment, the photocatalytic performance was higher than that of as-received powder. Enhancement of photocatalytic activities was discussed in relation to visible light absorption and charge carrier transfer.T.I., H.O. and D.H. were supported by a programme, the Strategic Research Foundation at Private Universities, grant no. S1311023, from Ministry of Education, Culture, Sports, Science and Technology (MEXT), Japan

Supplementation of protein-free diet with whey protein hydrolysates prevents skeletal muscle mass loss in rats

AbstractMuscle mass loss is induced by aging, several catabolic diseases, and malnutrition. It is well known that ingestion of whey protein and its hydrolysates (WPH) is effective in stimulating muscle protein synthesis. However, these studies focused on the acute up-regulation of muscle protein synthesis, and few studies have investigated the effect of whey protein and WPH on muscle mass during chronic malnutrition. The aim of the present study was to investigate the effect of 7 days supplementation of whey protein and WPH on muscle reduction in Wistar rats fed a protein-free (PF) diet. Wistar rats were fed either a standard diet (containing 20% protein) or a PF diet during the experimental period. Those fed a PF diet received a dietary supplement containing an amino acid mixture, whey protein, or WPH for 7 days. The weight of the extensor digitorum longus decreased in rats fed a PF diet supplemented with the amino acid mixture or the whey protein. However, this decrease was partially but significantly suppressed in the group fed the WPH supplement. Additionally, administration of WPH induced a postprandial increase in plasma essential amino acids, branched-chain amino acids, and leucine concentration compared with animals fed the amino acid mixture or the whey protein. These results suggest that 7 days supplementation of the diet with WPH suppressed muscle weight loss in rats fed a PF diet

LÍNGUA INGLESA E SOCIABILIZAÇÃO JUVENIL: UMA INTERLOCUÇÃO ENTRE UNESPAR E EDHUCCA – Escola de Desenvolvimento Humano “Casa do Caminho”

O desenvolvimento linguístico-cultural, o respeito e a valorização do adolescente em situação de vulnerabilidade social é o princípio norteador do projeto de extensão “Oficina linguístico-cultural na EDHUCCA – Escola de Desenvolvimento Humano “Casa do Caminho”, o qual tem sido executado por uma docente e quatro acadêmicos do curso de Licenciatura em Letras Inglês, desde o mês de março de 2018, no campus de Apucarana. A EDHUCCA é uma entidade sem fins lucrativos que desenvolve várias ações com famílias em situação de risco ou vulnerabilidade social, dentre as quais, destaca-se o projeto de sociabilização infanto-juvenil. Inserido neste contexto, o objetivo geral de nosso projeto é promover uma oficina semanal, de apoio escolar, quanto ao conhecimento sistêmico/gramatical, leitura, produção escrita e oralidade da língua inglesa para a sociabilização de adolescentes atendidos pela EDHUCCA. Dado o contexto de exclusão/inclusão social dos 10 adolescentes, atualmente participantes do projeto, a metodologia de trabalho adotada para o ensino da língua inglesa na oficina ancora-se na perspectiva de ensino e aprendizagem da Pedagogia Histórico-Crítica, a qual organiza didaticamente a transposição didática dos conteúdos linguístico-culturais em cinco etapas: prática social inicial, problematização, instrumentalização, catarse e prática social final. Assim, esperamos que os adolescentes do projeto apropriem-se do que é socialmente necessário para formá-los cidadãos conscientes, críticos e participativos na sociedade. Com o desenvolvimento dessa ação extensionista, almejamos contribuir para a formação linguístico-cultural e cidadã dos adolescentes, bem como para a educação profissional de professores de língua inglesa em formação inicial, permitindo-lhes uma experiência da docência no âmbito da educação não formal. Por fim, entendemos que o contexto do projeto e as atividades desenvolvidas constituem-se como um lócus de investigação significativo para a produção de novos conhecimentos acerca do ensino-aprendizagem de línguas

Increased accumulation of cytosine arabinoside in human leukemic cells and enhancement of its cell-killing activity by uridine.

The effects of uridine(UR) on the cell-killing activity of cytosine arabinoside(ara-C) against human leukemic cells, MOLT-4, and on ara-C accumulation in cells were studied. The 50% lethal dose(LD50) of ara-C as determined by clonogenic assay was decreased to 5.0 x 10(-8) mol from 9.0 x 10(-7) mol after 3 days exposure to 10(-3) mol of UR. The accumulation of 3H-ara-C at 24 and 48 h was significantly increased in culture medium containing 10(-8) mol of 3H-ara-C and 10(-3) mol of UR (5,129 +/- 123.5 vs 2,554 +/- 115.5 cpm/10(5) cells at 24 h, p less than 0.01, and 5,772 +/- 123.2 vs 1,372 +/- 51.8 cpm/10(5) cells at 48 h, p less than 0.01). It is noteworthy that cell-killing activity of ara-C against human leukemic cells was enhanced by the combination with a nucleoside(UR), but not with antileukemic agents.</p

Downregulation of SAV1 plays a role in pathogenesis of high-grade clear cell renal cell carcinoma

<p>Abstract</p> <p>Background</p> <p>Clinical outcome of patients with high-grade ccRCC (clear cell renal cell carcinoma) remains still poor despite recent advances in treatment strategies. Molecular mechanism of pathogenesis in developing high-grade ccRCC must be clarified. In the present study, we found that SAV1 was significantly downregulated with copy number loss in high-grade ccRCCs. Therefore, we investigated the SAV1 function on cell proliferation and apoptosis in vitro. Furthermore, we attempted to clarify the downstream signaling which is regulated by SAV1.</p> <p>Methods</p> <p>We performed array CGH and gene expression analysis of 8 RCC cell lines (786-O, 769-P, KMRC-1, KMRC-2, KMRC-3, KMRC-20, TUHR4TKB, and Caki-2), and expression level of mRNA was confirmed by quantitative RT-PCR (qRT-PCR) analysis. We next re-expressed SAV1 in 786-O cells, and analyzed its colony-forming activity. Then, we transfected siRNAs of SAV1 into the kidney epithelial cell line HK2 and renal proximal tubule epithelial cells (RPTECs), and analyzed their proliferation and apoptosis. Furthermore, the activity of YAP1, which is a downstream molecule of SAV1, was evaluated by western blot analysis, reporter assay and immunohistochemical analysis.</p> <p>Results</p> <p>We found that SAV1, a component of the Hippo pathway, is frequently downregulated in high-grade ccRCC. SAV1 is located on chromosome 14q22.1, where copy number loss had been observed in 7 of 12 high-grade ccRCCs in our previous study, suggesting that gene copy number loss is responsible for the downregulation of SAV1. Colony-forming activity by 786-O cells, which show homozygous loss of SAV1, was significantly reduced when SAV1 was re-introduced exogenously. Knockdown of SAV1 promoted proliferation of HK2 and RPTEC. Although the phosphorylation level of YAP1 was low in 786-O cells, it was elevated in SAV1-transduced 786-O cells. Furthermore, the transcriptional activity of the YAP1 and TEAD3 complex was inhibited in SAV1-transduced 786-O cells. Immunohistochemistry frequently demonstrated nuclear localization of YAP1 in ccRCC cases with SAV1 downregulation, and it was preferentially detected in high-grade ccRCC.</p> <p>Conclusions</p> <p>Taken together, downregulation of SAV1 and the consequent YAP1 activation are involved in the pathogenesis of high-grade ccRCC. It is an attractive hypothesis that Hippo signaling could be candidates for new therapeutic target.</p

Aclarubicin in the treatment of elderly patients with acute nonlymphocytic leukemia.

Thirteen previously untreated patients aged 70 and above with acute nonlymphocytic leukemia were treated with aclarubicin (ACR) alone. Among 10 cases (3, acute myelocytic leukemia; 4, acute myelomonocytic leukemia; 2, acute monocytic leukemia; and one, acute erythroleukemia) in which an evaluation was possible, 5 cases (3, acute myelomonocytic leukemia; and 2, acute monocytic leukemia) obtained complete remission (CR). The CR rate was 83% in 6 patients with acute myelomonocytic leukemia or acute monocytic leukemia. The median CR duration and survival was 7.5 and 10 + months, respectively. Although side effects of the drug on digestive system such as nausea, vomiting and anorexia were observed in all patients, they were controllable by conventional treatments. The results suggest that ACR is effective for the clinical management of elderly patients with acute nonlymphocytic leukemia, especially those with acute myelomonocytic leukemia or acute monocytic leukemia.</p

The Japanese Clinical Practice Guideline for acute kidney injury 2016

Acute kidney injury (AKI) is a syndrome which has a broad range of etiologic factors depending on different clinical settings. Because AKI has significant impacts on prognosis in any clinical settings, early detection and intervention are necessary to improve the outcomes of AKI patients. This clinical guideline for AKI was developed by a multidisciplinary approach with nephrology, intensive care medicine, blood purification, and pediatrics. Of note, clinical practice for AKI management which was widely performed in Japan was also evaluated with comprehensive literature search

Protective effect of geranylgeranylacetone, an inducer of heat shock protein 70, against drug-induced lung injury/fibrosis in an animal model

<p>Abstract</p> <p>Background</p> <p>To determine whether oral administration of geranylgeranylacetone (GGA), a nontoxic anti-ulcer drug that is an inducer of heat shock protein (HSP) 70, protects against drug-induced lung injury/fibrosis <it>in vivo</it>.</p> <p>Methods</p> <p>We used a bleomycin (BLM)-induced lung fibrosis model in which mice were treated with oral 600 mg/kg of GGA before and after BLM administration. Inflammation and fibrosis were evaluated by histological scoring, hydroxyproline content in the lung and inflammatory cell count, and quantification by ELISA of macrophage inflammatory protein-2 (MIP-2) in bronchoalveolar lavage fluid. Apoptosis was evaluated by the TUNEL method. The induction of HSP70 in the lung was examined with western blot analysis and its localization was determined by immunohistochemistry.</p> <p>Results</p> <p>We confirmed the presence of inflammation and fibrosis in the BLM-induced lung injury model and induction of HSP70 by oral administration of GGA. GGA prevented apoptosis of cellular constituents of lung tissue, such as epithelial cells, most likely related to the <it>de novo </it>induction of HSP70 in the lungs. GGA-treated mice also showed less fibrosis of the lungs, associated with the findings of suppression of both production of MIP-2 and inflammatory cell accumulation in the injured lung, compared with vehicle-treated mice.</p> <p>Conclusion</p> <p>GGA had a protective effect on drug-induced lung injury/fibrosis. Disease-modifying antirheumatic drugs such as methotrexate, which are indispensable for the treatment of rheumatoid arthritis, often cause interstitial lung diseases, an adverse event that currently cannot be prevented. Clinical use of GGA for drug-induced pulmonary fibrosis might be considered in the future.</p