Surface functionalization of 3D printed structures: Aesthetic and antibiofouling properties

Additive manufacturing (AM) is a hot topic nowadays, having a first order in importance in research trends, improving existent technologies and carrying them further. AM can be applied to ceramics, which have importance in current technologies. Their capability to maintain functional properties for long time periods, combined with the easiness to process and the abundance of raw materials, make them a fundamental part of mankind development. Within ceramics, stoneware has a wide range of uses but in some conditions, it can be affected by biofouling. Ti(O)N and Ag-Ti(O)N coatings over 3D printed stoneware, were presented as multifunctional solution, linking aesthetical and antimicrobial properties. Films were developed by reactive direct current (DC) magnetron sputtering and characterized physical, chemical and morphologically, as well as regarding their colour variation. Moreover roughness, wettability, antibacterial and antibiofouling were also evaluated. The results revealed that the Ag doped coatings (with or without oxygen addition) had an enhanced multifunctionality compared to control samples (without Ag). Ag nanoparticles addition created a surface with potential antibacterial and antibiofouling activities, in order to resist outdoors and aqueous environments, making these films able to be applied in architectural pieces as sculptures or other decorative parts, maintaining their properties with good aesthetical properties.The authors acknowledge to MIT Portugal-2017 program by thefinancial support through FCT/MCTES for this exploratory researchproject with the reference MIT-EXPL/ISF/0006/2007 and PhysicsCenter of University of Minho and University of Porto (CFUM-UP) by itssupport though the strategical project (UID/FIS/04650/2019). Thisstudy was supported by the Portuguese Foundation for Science andTechnology (FCT) under the scope of the strategic funding of UID/FIS/04650/2019 and UID/BIO/04469/2019 unit and BioTecNorte opera-tion (NORTE-01-0145-FEDER-000004) funded by the EuropeanRegional Development Fund under the scope of Norte2020—ProgramaOperacional Regional do Norte and, in the framework of the ATRITO-0(co-financed via FEDER (PT2020) POCI-01-0145-FEDER-030446 andFCT (PIDDAC)) and the On-SURF (co-financedvia FEDER (PT2020)POCI-01-0247-FEDER-024521) projects.info:eu-repo/semantics/publishedVersio

Esquizofrenia e cannabis: Qual a relação?

RESUMO: A droga ilícita mais consumida no mundo, entre pessoas de 15 a 64 anos, é a maconha. Estudos epidemiológicos apontam uma possível associação causal entre esse ativo, oriundo do gênero cannabis, e a esquizofrenia. Há muita especulação quanto aos impactos dessa droga sobre a psicose esquizofrênica. Posto a relevância do assunto, o objetivo dessa revisão foi integrar as informações presentes na literatura, visando investigar possíveis associações entre o uso de cannabis e esquizofrenia. O uso de cannabis foi analisado quanto a possibilidade de favorecer o desenvolvimento de esquizofrenia em pacientes previamente hígidos, e, quanto a possibilidade de atenuar ou agravar a sintomatologia apresentada por pacientes com o transtorno psicótico. Como metodologia, foi realizada pesquisa de livros e artigos internacionais entre fevereiro e março de 2020, realizada nos documentos indexados encontrados nas bases de dados National Library of Medicine and National Institutes of Health (PUBMED), Literatura Latino- Americana e do Caribe em Ciências da Saúde (LILACS). A combinação dos descritores em inglês: “schizophrenia” e “cannabis” identificaram 44 artigos, e dentre esses, 15 foram incluídos nessa revisão. Conclui-se que, as referências utilizadas demonstraram evidências de que a maconha é um dos fatores que aumentam o risco de desenvolvimento de esquizofrenia. Diante disso, quanto aos resultados, eles demonstraram evidências que corroboram que a maconha é um dos fatores que aumentam o risco de desenvolvimento de esquizofrenia. Quanto à exposição da Cannabis em indivíduos que são portadores do transtorno esquizofrênico, os resultados dividem-se em duas frentes: os possíveis efeitos nocivos e os possíveis efeitos terapêuticos (farmacológicos)

Neuroplasticidade e estilo de vida: qual a relação?

RESUMO: Essa revisão teve como fundamento o gradativo rompimento do pensamento de que o cérebro é um conjunto de multiestruturas isoladas permitiu a estruturação de um novo conceito: o cérebro é um órgão dinâmico e adaptável frente às exigências impostas ao mesmo. Diante desse cenário, a neuroplasticidade ganha relevância, posto que, de acordo com C. H. Phelp (1990), trata-se de uma mudança adaptativa estrutural e funcional do sistema nervoso, que “ocorre em qualquer estágio da ontogenia, como função de interações com o ambiente interno ou externo ou, ainda, como resultado de injúrias, de traumatismos ou de lesões que afetam o ambiente neural”. Teve como objetivo revisar possíveis associações entre neuroplasticidade e estilo de vida. Apresntou como metodologia a busca de livros e artigos, nacionais e internacionais, utilizando a Biblioteca Virtual em Saúde – BVS MS e o PubMed. Ultilizou-se como descritores: plasticidade neuronal, exercícios aeróbicos, yoga, e estilo de vida. 12 artigos foram selecionados e revisados, mas apenas 7 foram incluídos. Teve como resultados mais significativos encontradas referentes à estilo de vida, yoga e exercícios aeróbicos, ao lado da demonstração da relação entre neuroplasticidade e patologia de Alzheimer. Conclui-se que há relação entre neuroplasticidade e estilo de vida, porém, há diminuta amostragem de estudos sobre a temática. Ainda, os mecanismos que demonstram o vínculo descrito são pouco compreendidos, inferindo e demandando maior volume de estudos esclarecedores sobre a temática. &nbsp

Cancer health disparities in racial/ethnic minorities in the United States

There are well-established disparities in cancer incidence and outcomes by race/ethnicity that result from the interplay between structural, socioeconomic, socio-environmental, behavioural and biological factors. However, large research studies designed to investigate factors contributing to cancer aetiology and progression have mainly focused on populations of European origin. The limitations in clinicopathological and genetic data, as well as the reduced availability of biospecimens from diverse populations, contribute to the knowledge gap and have the potential to widen cancer health disparities. In this review, we summarise reported disparities and associated factors in the United States of America (USA) for the most common cancers (breast, prostate, lung and colon), and for a subset of other cancers that highlight the complexity of disparities (gastric, liver, pancreas and leukaemia). We focus on populations commonly identified and referred to as racial/ethnic minorities in the USA—African Americans/Blacks, American Indians and Alaska Natives, Asians, Native Hawaiians/other Pacific Islanders and Hispanics/Latinos. We conclude that even though substantial progress has been made in understanding the factors underlying cancer health disparities, marked inequities persist. Additional efforts are needed to include participants from diverse populations in the research of cancer aetiology, biology and treatment. Furthermore, to eliminate cancer health disparities, it will be necessary to facilitate access to, and utilisation of, health services to all individuals, and to address structural inequities, including racism, that disproportionally affect racial/ethnic minorities in the USA.Fil: Zavala, Valentina A.. University of California; Estados UnidosFil: Bracci, Paige M.. University of California; Estados UnidosFil: Carethers, John M.. University of Michigan; Estados UnidosFil: Carvajal Carmona, Luis. University of California at Davis; Estados UnidosFil: Coggins, Nicole B.. University of California at Davis; Estados UnidosFil: Cruz Correa, Marcia R.. Universidad de Puerto Rico; Puerto RicoFil: Davis, Melissa. No especifíca;Fil: de Smith, Adam J.. University of California; Estados UnidosFil: Dutil, Julie. Ponce Research Institute; Puerto RicoFil: Figueiredo, Jane C.. Cedars Sinai Medical Center; Estados UnidosFil: Fox, Rena. University of California; Estados UnidosFil: Graves, Kristi D.. University Of Georgetown; Estados UnidosFil: Gomez, Scarlett Lin. University of California; Estados UnidosFil: Llera, Andrea Sabina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Bioquímicas de Buenos Aires. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas de Buenos Aires; ArgentinaFil: Neuhausen, Susan L.. No especifíca;Fil: Newman, Lisa. No especifíca;Fil: Nguyen, Tung. University of California; Estados UnidosFil: Palmer, Julie R.. National Institutes of Health; Estados UnidosFil: Palmer, Nynikka R.. University of California; Estados UnidosFil: Pérez Stable, Eliseo J.. National Institutes of Health; Estados UnidosFil: Piawah, Sorbarikor. University of California; Estados UnidosFil: Rodriquez, Erik J.. National Institutes of Health; Estados UnidosFil: Sanabria Salas, María Carolina. Instituto Nacional de Cancerología; ColombiaFil: Schmit, Stephanie L.. University of Southern California; Estados UnidosFil: Serrano Gomez, Silvia J.. Instituto Nacional de Cancerología; ColombiaFil: Stern, Mariana Carla. University of Southern California; Estados UnidosFil: Weitzel, Jeffrey. No especifíca;Fil: Yang, Jun J.. St. Jude Children’s Research Hospital; Estados UnidosFil: Zabaleta, Jovanny. No especifíca;Fil: Ziv, Elad. University of California; Estados UnidosFil: Fejerman, Laura. University of California; Estados Unido

A Genetic Locus within the FMN1/GREM1 Gene Region Interacts with Body Mass Index in Colorectal Cancer Risk

Colorectal cancer risk can be impacted by genetic, environmental, and lifestyle factors, including diet and obesity. Geneenvironment interactions (G x E) can provide biological insights into the effects of obesity on colorectal cancer risk. Here, we assessed potential genome-wide G x E interactions between body mass index (BMI) and common SNPs for colorectal cancer risk using data from 36,415 colorectal cancer cases and 48,451 controls from three international colorectal cancer consortia (CCFR, CORECT, and GECCO). The G x E tests included the conventional logistic regression using multiplicative terms (one degree of freedom, 1DF test), the two-step EDGE method, and the joint 3DF test, each of which is powerful for detecting G x E interactions under specific conditions. BMI was associated with higher colorectal cancer risk. The two-step approach revealed a statistically significant GxBMI interaction located within the Formin 1/Gremlin 1 (FMN1/GREM1) gene region (rs58349661). This SNP was also identified by the 3DF test, with a suggestive statistical significance in the 1DF test. Among participants with the CC genotype of rs58349661, overweight and obesity categories were associated with higher colorectal cancer risk, whereas null associations were observed across BMI categories in those with the TT genotype. Using data from three large international consortia, this study discovered a locus in the FMN1/GREM1 gene region that interacts with BMI on the association with colorectal cancer risk. Further studies should examine the potential mechanisms through which this locus modifies the etiologic link between obesity and colorectal cancer

Novel Common Genetic Susceptibility Loci for Colorectal Cancer

BACKGROUND: Previous genome-wide association studies (GWAS) have identified 42 loci (P < 5 × 10-8) associated with risk of colorectal cancer (CRC). Expanded consortium efforts facilitating the discovery of additional susceptibility loci may capture unexplained familial risk. METHODS: We conducted a GWAS in European descent CRC cases and control subjects using a discovery-replication design, followed by examination of novel findings in a multiethnic sample (cumulative n = 163 315). In the discovery stage (36 948 case subjects/30 864 control subjects), we identified genetic variants with a minor allele frequency of 1% or greater associated with risk of CRC using logistic regression followed by a fixed-effects inverse variance weighted meta-analysis. All novel independent variants reaching genome-wide statistical significance (two-sided P < 5 × 10-8) were tested for replication in separate European ancestry samples (12 952 case subjects/48 383 control subjects). Next, we examined the generalizability of discovered variants in East Asians, African Americans, and Hispanics (12 085 case subjects/22 083 control subjects). Finally, we examined the contributions of novel risk variants to familial relative risk and examined the prediction capabilities of a polygenic risk score. All statistical tests were two-sided. RESULTS: The discovery GWAS identified 11 variants associated with CRC at P < 5 × 10-8, of which nine (at 4q22.2/5p15.33/5p13.1/6p21.31/6p12.1/10q11.23/12q24.21/16q24.1/20q13.13) independently replicated at a P value of less than .05. Multiethnic follow-up supported the generalizability of discovery findings. These results demonstrated a 14.7% increase in familial relative risk explained by common risk alleles from 10.3% (95% confidence interval [CI] = 7.9% to 13.7%; known variants) to 11.9% (95% CI = 9.2% to 15.5%; known and novel variants). A polygenic risk score identified 4.3% of the population at an odds ratio for developing CRC of at least 2.0. CONCLUSIONS: This study provides insight into the architecture of common genetic variation contributing to CRC etiology and improves risk prediction for individualized screenin