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1.
J Clin Med ; 13(12)2024 Jun 12.
Artigo em Inglês | MEDLINE | ID: mdl-38929962

RESUMO

Background. The objective of this systematic review and meta-analysis was to estimate the proportions of individuals infected with Campylobacter, Escherichia, Salmonella, Shigella, or Yersinia who develop reactive arthritis. Methods. A systematic review was conducted, encompassing English-language articles published before January 2024, sourced from the Embase, PubMed, Scopus, and Web of Science databases. This review included observational studies that reported the occurrence of reactive arthritis (ReA) among patients with Campylobacter, Escherichia, Salmonella, Shigella, or Yersinia infections. Data extraction was carried out independently by two reviewers. Subsequently, a random-effects meta-analysis was performed, with heterogeneity assessed using the I2 value. Additionally, meta-regression was employed to investigate the potential influence of study-level variables on the observed heterogeneity. Results. A total of 87 studies were identified; 23 reported on ReA development after Campylobacter infection, 7 reported on ReA after Escherichia infection, 30 reported ReA onset after salmonellosis, 14 reported ReA after shigellosis, and 13 reported ReA after Yersinia infection. The proportion of Campylobacter patients who developed ReA was 0.03 (95% CI [0.01, 0.06], I2 = 97.62%); the proportion of Escherichia patients who developed ReA was 0.01 (95% CI [0.00, 0.06], I2 = 92.78%); the proportion of Salmonella patients was 0.04 (95% CI [0.02, 0.08], I2 = 97.67%); the proportion of Shigella patients was 0.01 (95% CI [0.01, 0.03], I2 = 90.64%); and the proportion of Yersinia patients who developed ReA was 0.05 (95% CI [0.02, 0.13], I2 = 96%). Conclusion. A significant proportion of Salmonella, Shigella, and Yersinia cases resulted in ReA. Nonetheless, it is important to interpret the findings cautiously due to the substantial heterogeneity observed between studies.

2.
Int J Pharm ; 647: 123528, 2023 Nov 25.
Artigo em Inglês | MEDLINE | ID: mdl-37863449

RESUMO

In the contemporary era, microorganisms, spanning bacteria and viruses, are increasingly acknowledged as emerging contaminants in the environment, presenting significant risks to public health. Nevertheless, conventional methods for disinfecting these microorganisms are often ineffective. Additionally, they come with disadvantages such as high energy usage, negative environmental consequences, increased expenses, and the generation of harmful byproducts. The development of next-generation antifungal and antibacterial agents is dependent on newly synthesized nanomaterials with inherent antimicrobial behavior. In this study, we report an arc-discharge method to synthesize MoOx nanosheets and microbelts, followed by decorating them with ultrafine Ag nanoparticles (NPs). Scanning and transmission electron microscopies show that Ag NPs formation on the Molybdenum oxide nanostructures rolls them into nanotube caps (NTCs), revealing inner and outer diameters of approximately 19.8 nm and 105.5 nm, respectively. Additionally, the Ag NPs are ultrafine, with sizes in the range of 5-8 nm. Results show that the prepared NTCs exhibit dose-dependent sensitivity to both planktonic and biofilm cells of Escherichia coli and Candida albicans. The anti-biofilm activity in terms of biofilm inhibition ranged from 19.7 to 77.2% and 11.3-82.3%, while removal of more than 70% and 90% of preformed biofilms was achieved for E. coli and C. albicans, respectively, showing good potential for antimicrobial coating. Initial MoOx exhibits positive potential, while Ag-decorated Molybdenum oxide NTCs show dual potential effects (positive for Molybdenum oxide NTCs and negative for Ag NPs. Molybdenum oxide NTCs, with their strong positive potential, efficiently attract microbes due to their negatively charged cell surfaces, facilitating the antimicrobial effect of Ag NPs, leading to cell damage and death. These findings suggest that the synthesized NPs could serve as a suitable coating for biomedical applications.


Assuntos
Anti-Infecciosos , Nanopartículas Metálicas , Nanotubos , Nanopartículas Metálicas/química , Escherichia coli , Óxidos , Prata/farmacologia , Prata/química , Anti-Infecciosos/farmacologia , Anti-Infecciosos/química , Antibacterianos/farmacologia , Antibacterianos/química , Testes de Sensibilidade Microbiana
3.
Mol Cancer ; 22(1): 90, 2023 05 31.
Artigo em Inglês | MEDLINE | ID: mdl-37259089

RESUMO

Epithelial mesenchymal transition (EMT) and mesenchymal epithelial transition (MET) are genetic determinants of cellular plasticity. These programs operate in physiological (embryonic development, wound healing) and pathological (organ fibrosis, cancer) conditions. In cancer, EMT and MET interfere with various signalling pathways at different levels. This results in gross alterations in the gene expression programs, which affect most, if not all hallmarks of cancer, such as response to proliferative and death-inducing signals, tumorigenicity, and cell stemness. EMT in cancer cells involves large scale reorganisation of the cytoskeleton, loss of epithelial integrity, and gain of mesenchymal traits, such as mesenchymal type of cell migration. In this regard, EMT/MET plasticity is highly relevant to the Go-or-Grow concept, which postulates the dichotomous relationship between cell motility and proliferation. The Go-or-Grow decisions are critically important in the processes in which EMT/MET plasticity takes the central stage, mobilisation of stem cells during wound healing, cancer relapse, and metastasis. Here we outline the maintenance of quiescence in stem cell and metastatic niches, focusing on the implication of EMT/MET regulatory networks in Go-or-Grow switches. In particular, we discuss the analogy between cells residing in hybrid quasi-mesenchymal states and GAlert, an intermediate phase allowing quiescent stem cells to enter the cell cycle rapidly.


Assuntos
Transição Epitelial-Mesenquimal , Neoplasias , Humanos , Diferenciação Celular , Divisão Celular , Transição Epitelial-Mesenquimal/genética , Neoplasias/genética , Neoplasias/patologia , Transdução de Sinais
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