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1.
J Med Microbiol ; 70(10)2021 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-34633919

RESUMO

Antifungal drugs have already been established as an effective treatment option for Candida parapsilosis infections, but there is no universal consensus on the ideal target for clinical efficacy and safety of antifungal drugs for the treatment of C. parapsilosis infections. Few studies have directly compared the efficacies of antifungal drugs for the treatment of C. parapsilosis infections. We hypothesize that different antifungal drugs offer differing clinical efficacy and safety for the treatment of C. parapsilosis infections. We performed a comprehensive network meta-analysis on different strategies for C. parapsilosis infection treatment and compared the clinical efficacy and safety of antifungal drugs as interventions for C. parapsilosis infections. The Cochrane Database of Systematic Reviews, Medline, Embase, PubMed, Web of Science, China National Knowledge Infrastructure (CNKI), Technology of Chongqing VIP database, Wan Fang Data, and SinoMed databases were searched to identify appropriate randomized trials. Among the extracted C. parapsilosis cases, the survival and death rates with treatment of C. parapsilosis infection were compared among groups treated with different antifungal drugs. According to the evidence-network analysis, echinocandins were a better choice than other drugs for treating C. parapsilosis infections, and more importantly, caspofungin showed a more preferable effect for decreasing the risk of 30 day mortality. In conclusion, this study systematically evaluated the effectiveness and safety of antifungal drugs for the purpose of helping clinicians choose the most appropriate antifungal drugs. Future studies with larger samples are needed to evaluate the effects of patient factors on the clinical efficacy and safety of antifungal drugs for C. parapsilosis infections.


Assuntos
Antifúngicos/uso terapêutico , Candida parapsilosis/efeitos dos fármacos , Candidíase/tratamento farmacológico , Monitoramento de Medicamentos , Adulto , Idoso , Idoso de 80 Anos ou mais , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Resultado do Tratamento
2.
Biomed Pharmacother ; 101: 769-776, 2018 May.
Artigo em Inglês | MEDLINE | ID: mdl-29524886

RESUMO

Substantial evidence has demonstrated the involvement of long non-coding RNAs (lncRNAs) in the development and progression of colorectal cancer (CRC) via their regulation on cancer cell proliferation, apoptosis, invasion and metastasis pathways. The current study aimed to understand the role of lncRNA Linc00675 in the progression and metastasis of CRC and to identify the potential lncRNA-miRNA interactions and signaling pathways underlying the mechanisms of action of Linc00675 in CRC. Our data firstly demonstrated the down-regulation of Linc00675 in both CRC cells and clinical CRC tissues. Expression of Linc00675 was also relatively low in metastatic tumors and advanced tumors. Further studies also showed that overexpression of Linc00675 inhibited the proliferation, invasion and migration of CRC cells. In addition, our data also revealed the negative regulation of miR-942 by Linc00675 and the relatively higher expression of miR-942 in clinical CRC tissues. More importantly, the inhibitory effect of Linc00675 on proliferation, invasion and migration of HCT116 cells was also significantly attenuated in the presence of miR-942 mimic, suggesting that down-regulation of miR-942 represented one of the mechanisms by which Linc00675 inhibited the proliferation and metastasis of CRC. Furthermore, we also demonstrated the inhibition of Wnt/ß-catenin signaling in the Linc00675/miR-942 regulated pathway in CRC cells. Taken together, our findings suggested Linc00675 as a potential molecular marker and target for the diagnosis and treatment of CRC and enhanced the current understanding on the mechanisms of action of Linc00675 in CRC.


Assuntos
Proliferação de Células/fisiologia , Neoplasias Colorretais/metabolismo , MicroRNAs/metabolismo , RNA Longo não Codificante/biossíntese , Via de Sinalização Wnt/fisiologia , beta Catenina/metabolismo , Movimento Celular/fisiologia , Neoplasias Colorretais/patologia , Neoplasias Colorretais/prevenção & controle , Células HCT116 , Humanos , MicroRNAs/antagonistas & inibidores , Invasividade Neoplásica/patologia , Invasividade Neoplásica/prevenção & controle , beta Catenina/antagonistas & inibidores
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