Modelo de avaliação do capital intelectual de empresas de transportes de cargas e logística por meio da metodologia InCaS

TCC (graduação) - Universidade Federal de Santa Catarina. Campus Joinville. Engenharia de Transportes e Logística.A pandemia de COVID -19, além de causar perdas de vidas, afetou diretamente a economia mundial e forçou as empresas a se adaptarem neste novo contexto, buscando melhorias e otimização dos seus processos através de vantagens competitivas como conhecimento e inovação. A inovação combinada com capital intelectual tem crescido nos últimos anos, pois além de identificar oportunidades e ameaças no mercado, é capaz de identificar internamente as competências corporativas e de recursos das empresas. Com a necessidade das empresas em melhorar o desenvolvimento de conhecimentos e habilidades, os ativos imateriais tornam-se mais relevantes, considerando habilidades, processos organizacionais, informação e conhecimento. Com isso, surge a necessidade de desenvolver um modelo que permita as empresas avaliar um conjunto de conhecimentos, informações e recursos que compõem o capital intelectual. Uma ferramenta para a avaliação de capital intelectual é a metodologia InCaS – Intellectual Capital Statement – que desdobra este capital em humano, relacional e estrutural. Assim, este trabalho propõe um modelo para avaliar o capital intelectual de empresas de transportes de cargas e logística utilizando a metodologia InCaS, a fim de identificar os critérios intangíveis e apresentar os conhecimentos da área de transporte e logística de acordo com os capitais intelectuais. Ao fim, o modelo foi aplicado em uma empresa da área de transportes de carga e logística de Joinville, confirmando que o modelo é válido

Optimization of Light-Inducible Gal4/UAS Gene Expression System in Mammalian Cells

遺伝子発現を光で制御できる新技術を開発 --発生・幹細胞研究への貢献に期待--. 京都大学プレスリリース. 2020-08-28.Light-inducible gene expression systems represent powerful methods for studying the functional roles of dynamic gene expression. Here, we developed an optimized light-inducible Gal4/UAS gene expression system for mammalian cells. We designed photoactivatable (PA)-Gal4 transcriptional activators based on the concept of split transcription factors, in which light-dependent interactions between Cry2-CIB1 PA-protein interaction modules can reconstitute a split Gal4 DNA-binding domain and p65 transcription activation domain. We developed a set of PA-Gal4 transcriptional activators (PA-Gal4cc), which differ in terms of induced gene expression levels following pulsed or prolonged light exposure, and which have different activation/deactivation kinetics. These systems offer optogenetic tools for the precise manipulation of gene expression at fine spatiotemporal resolution in mammalian cells

A five-step synthesis of psilocin from indole-3-carbaldehyde

金沢大学大学院自然科学研究科生理活性物質科学金沢大学薬学部A novel preparative method of psilocin was established in only five steps from indole-3-carbaldehyde in 50% overall yield

Differential, histochemical and immunohistochemical changes in rat hepatocytes after isoflurane or sevoflurane exposure.

Differential, histochemical and immunohistochemical changes were observed in hepatocytes from immediately to 7 days after isoflurane or sevoflurane exposure (at H 0 to on Day 7) to study the process of development and recovery in anesthetic-induced hepatic injury. A total of 570 7-week-old male Sprague-Dawley rats with or without phenobarbital treatment were exposed to isoflurane or sevoflurane in 100%, 21%, or 10% oxygen, or to 10% oxygen alone for 2h. In phenobarbital-treated rats, hepatocytes both with and without anesthetic exposure markedly changed in 10% oxygen at H 0. Glycogen and ribosomal ribonucleic acid (rRNA) disappeared at H 0 and at H 6, respectively, and at H 6, AST levels in the blood rose. From H 6 to Day 1, necrosis developed more markedly and widely in zone 3 hepatocytes exposed to anesthetics in 10% oxygen than in those exposed to oxygen alone. All degenerated tissues had returned to normal levels by day 7. Recovery of the hepatolobular structure may be attributed to rearrangement of remaining hepatocytes in the portal vein area. Both the disappearance of glycogen and rRNA and the increase in blood AST levels after exposure to isoflurane or sevoflurane are considered to be factors contributing to the induction of necrosis around the central vein. The grade of isoflurane-induced hepatic injury was found to be significantly higher than that of sevoflurane.</p

Carbon-Ion Irradiation Suppresses Migration and Invasiveness of Human Pancreatic Carcinoma Cells MIAPaCa-2 via Rac1 and RhoA Degradation

PurposeTo investigate the mechanisms underlying the inhibition of cancer cell migration and invasion by carbon (C)-ion irradiation.Methods and MaterialsHuman pancreatic cancer cells MIAPaCa-2, AsPC-1, and BxPC-3 were treated by x-ray (4 Gy) or C-ion (0.5, 1, 2, or 4 Gy) irradiation, and their migration and invasion were assessed 2 days later. The levels of guanosine triphosphate (GTP)-bound Rac1 and RhoA were determined by the active GTPase pull-down assay with or without a proteasome inhibitor, and the binding of E3 ubiquitin ligase to GTP-bound Rac1 was examined by immunoprecipitation.ResultsCarbon-ion irradiation reduced the levels of GTP-bound Rac1 and RhoA, 2 major regulators of cell motility, in MIAPaCa-2 cells and GTP-bound Rac1 in AsPC-1 and BxPC-3 cells. Proteasome inhibition reversed the effect, indicating that C-ion irradiation induced Rac1 and RhoA degradation via the ubiquitin (Ub)-proteasome pathway. E3 Ub ligase X-linked inhibitor of apoptosis protein (XIAP), which directly targets Rac1, was selectively induced in C-ion–irradiated MIAPaCa-2 cells and coprecipitated with GTP-bound Rac1 in C-ion–irradiated cells, which was associated with Rac1 ubiquitination. Cell migration and invasion reduced by C-ion radiation were restored by short interfering RNA–mediated XIAP knockdown, indicating that XIAP is involved in C-ion–induced inhibition of cell motility.ConclusionIn contrast to x-ray irradiation, C-ion treatment inhibited the activity of Rac1 and RhoA in MIAPaCa-2 cells and Rac1 in AsPC-1 and BxPC-3 cells via Ub-mediated proteasomal degradation, thereby blocking the motility of these pancreatic cancer cells