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1.
Polymers (Basel) ; 16(6)2024 Mar 14.
Artigo em Inglês | MEDLINE | ID: mdl-38543414

RESUMO

This article will focus on the issue of protection against the pathogenic biofilm development on steel surfaces within the food sectors, highlighting steel's prominence as a material choice in these areas. Pathogenic microorganism-based biofilms present significant health hazards in the food industry. Current scientific research offers a variety of solutions to the problem of protecting metal surfaces in contact with food from the growth of pathogenic microorganisms. One promising strategy to prevent bacterial growth involves applying a polymeric layer to metal surfaces, which can function as either an antiadhesive barrier or a bactericidal agent. Thus, the review aims to thoroughly examine the application of antibacterial polymer coatings on steel, a key material in contact with food, summarizing research advancements in this field. The investigation into polymer antibacterial coatings is organized into three primary categories: antimicrobial agent-releasing coatings, contact-based antimicrobial coatings, and antifouling coatings. Antibacterial properties of the studied types of coatings are determined not only by their composition, but also by the methods for applying them to metal and coating surfaces. A review of the current literature indicates that coatings based on polymers substantially enhance the antibacterial properties of metallic surfaces. Furthermore, these coatings contribute additional benefits including improved corrosion resistance, enhanced aesthetic appeal, and the provision of unique design elements.

2.
Polymers (Basel) ; 15(20)2023 Oct 18.
Artigo em Inglês | MEDLINE | ID: mdl-37896381

RESUMO

Traditional butyl rubber halogenation technology involves the halogenation of IIR using molecular chlorine or bromine in a solution. However, this method is technologically complex. This study investigated a novel method for the halogenation of butyl rubber to enhance its stability and resistance to thermal oxidation and aggressive media. The butyl rubber was modified through mechanochemical modification, induced by solvent swelling in a polychlorinated n-alkane solution. During the modification, samples were obtained with chlorine content ranging from 3 to 15%. After extraction, the halogen content was quantitatively determined with the oxygen flask combustion method and X-ray photoelectron spectroscopy. It was shown that for samples with total chlorine content of up to 6%, there was almost no leaching of chlorine from the samples. The chemical structure of the extracted rubbers was ascertained using FT-IR and 1H NMR spectroscopy, and it was demonstrated that all samples showed absorption peaks and signals typical for chlorobutyl rubbers. It was observed that modification with polychlorinated n-alkanes improved the thermal and oxidative stability (the oxygen absorption rate decreased by 40%) and chemical resistance, estimated by the degree of swelling, which decreased with the increase in the chlorine content. This technology allows the production of a chlorinated rubber solution that can be directly used by rubber goods manufacturers and suppliers.

3.
Genes (Basel) ; 11(11)2020 11 13.
Artigo em Inglês | MEDLINE | ID: mdl-33202721

RESUMO

Filamin C (FLNC), being one of the major actin-binding proteins, is involved in the maintenance of key muscle cell functions. Inherited skeletal muscle and cardiac disorders linked to genetic variants in FLNC have attracted attention because of their high clinical importance and possibility of genotype-phenotype correlations. To further expand on the role of FLNC in muscle cells, we focused on detailed alterations of muscle cell properties developed after the loss of FLNC. Using the CRISPR/Cas9 method we generated a C2C12 murine myoblast cell line with stably suppressed Flnc expression. FLNC-deficient myoblasts have a significantly higher proliferation rate combined with an impaired cell migration capacity. The suppression of Flnc expression leads to inability to complete myogenic differentiation, diminished expression of Myh1 and Myh4, alteration of transcriptional dynamics of myogenic factors, such as Mymk and Myog, and deregulation of Hippo signaling pathway. Specifically, we identified elevated basal levels of Hippo activity in myoblasts with loss of FLNC, and ineffective reduction of Hippo signaling activity during myogenic differentiation. The latter was restored by Flnc overexpression. In summary, we confirmed the role of FLNC in muscle cell proliferation, migration and differentiation, and demonstrated for the first time the direct link between Flnc expression and activity of TEAD-YAP\TAZ signaling. These findings support a role of FLNC in regulation of essential muscle processes relying on mechanical as well as signaling mechanisms.


Assuntos
Filaminas/genética , Mioblastos/citologia , Transdução de Sinais/fisiologia , Aciltransferases/metabolismo , Proteínas Adaptadoras de Transdução de Sinal , Animais , Diferenciação Celular/genética , Linhagem Celular , Movimento Celular/genética , Proliferação de Células/genética , Fator de Crescimento do Tecido Conjuntivo/genética , Fator de Crescimento do Tecido Conjuntivo/metabolismo , Filaminas/metabolismo , Expressão Gênica , Técnicas de Inativação de Genes , Via de Sinalização Hippo , Camundongos , Desenvolvimento Muscular/genética , Proteínas Serina-Treonina Quinases/metabolismo , Proteínas de Sinalização YAP
4.
Front Genet ; 10: 608, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31297131

RESUMO

Even though genetic studies of individuals with neuromuscular diseases have uncovered the molecular background of many cardiac disorders such as cardiomyopathies and inherited arrhythmic syndromes, the genetic cause of a proportion of cardiomyopathies associated with neuromuscular phenotype still remains unknown. Here, we present an individual with a combination of cardiomyopathy and limb-girdle type muscular dystrophy where whole exome sequencing identified myoferlin (MYOF)-a member of the Ferlin protein family and close homolog of DYSF-as the most likely candidate gene. The disease-causative role of the identified variant c.[2576delG; 2575G>C], p.G859QfsTer8 is supported by functional studies in vitro using the primary patient's skeletal muscle mesenchymal progenitor cells, including both RNA sequencing and morphological studies, as well as recapitulating the muscle phenotype in vivo in zebrafish. We provide the first evidence supporting a role of MYOF in human muscle disease.

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