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1.
Surg Innov ; 30(1): 36-44, 2023 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-35507460

RESUMO

Background. Robotic systems can overcome some limitations of laparoscopic total mesorectal excision (L-TME), thus improving the quality of the surgery. So far, many studies have reported the technical feasibility and short-term oncological results of robotic total mesorectal excision (R-TME) in treating rectal cancer (RC); however, only a few evaluated the survival and long-term oncological outcomes. The following study compared the medium-term oncological data, 3-year overall survival (OS), and disease-free survival (DFS) of L-TME and R-TME in patients with rectal cancer. Methods. In this retrospective study, records of patients (patients with stage I-III rectal cancer) who underwent surgery (127 cases of L-TME and 148 cases of R-TME) at the Gansu Provincial Hospital between June 2016 and March 2018 were included in the analysis. Kaplan-Meier analysis evaluated the 3-year OS and DFS for all patients treated with curative intent. Results. The conversion rate was significantly higher, and the postoperative hospital stay was significantly longer in the L-TME group than in the R-TME group (all P<.05). Major complications were significantly lower in the robotic group (P<.05). The 3-year DFS rate (for all stages) was 74.8% for L-TME and 85.8% for R-TME (P = .021). For disease stage III, the 3-year DFS and OS were significantly higher in the R-TME group (P<.05). Conclusion. R-TME can achieve better oncological outcomes and is more beneficial for RC patients compared with L-TME, especially for those with stage III rectal cancers. Nevertheless, further randomized controlled trials and a longer follow-up period are needed to confirm these findings.


Assuntos
Laparoscopia , Neoplasias Retais , Procedimentos Cirúrgicos Robóticos , Robótica , Humanos , Procedimentos Cirúrgicos Robóticos/métodos , Estudos Retrospectivos , Laparoscopia/métodos , Neoplasias Retais/cirurgia , Resultado do Tratamento
2.
J Integr Plant Biol ; 54(12): 991-1006, 2012 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-23013333

RESUMO

The link between root growth, H2O2, auxin signaling, and the cell cycle in cadmium (Cd)-stressed rice (Oryza sativa L. cv. Zhonghua No. 11) was analyzed in this study. Exposure to Cd induced a significant accumulation of Cd, but caused a decrease in zinc (Zn) content which resulted from the decreased expression of OsHMA9 and OsZIP. Analysis using a Cd-specific probe showed that Cd was mainly localized in the meristematic zone and vascular tissues. Formation and elongation of the root system were significantly promoted by 3-amino-1,2,4-triazole (AT), but were markedly inhibited by N,N'-dimethylthiourea (DMTU) under Cd stress. The effect of H2O2 on Cd-stressed root growth was further confirmed by examining a gain-of-function rice mutant (carrying catalase1 and glutathione-S-transferase) in the presence or absence of diphenylene iodonium. DR5-GUS staining revealed close associations between H2O2 and the concentration and distribution of auxin. H2O2 affected the expression of key genes, including OsYUCCA, OsPIN, OsARF, and OsIAA, in the auxin signaling pathway in Cd-treated plants. These results suggest that H2O2 functions upstream of the auxin signaling pathway. Furthermore, H2O2 modified the expression of cell-cycle genes in Cd-treated roots. The effects of H2O2 on root system growth are therefore linked to auxin signal modification and to variations in the expression of cell-cycle genes in Cd-stressed rice. A working model for the effects of H2O2 on Cd-stressed root system growth is thus proposed and discussed in this paper.


Assuntos
Cádmio/toxicidade , Genes cdc , Peróxido de Hidrogênio/farmacologia , Ácidos Indolacéticos/metabolismo , Oryza/genética , Raízes de Plantas/efeitos dos fármacos , Transdução de Sinais/efeitos dos fármacos , Oryza/citologia , Raízes de Plantas/crescimento & desenvolvimento , Raízes de Plantas/metabolismo
3.
Zhonghua Zhong Liu Za Zhi ; 31(1): 28-32, 2009 Jan.
Artigo em Chinês | MEDLINE | ID: mdl-19538865

RESUMO

OBJECTIVE: The aim of this study was to investigate the expression of transforming growth factor-beta1 (TGF-beta1) and its signaling pathway molecules in oral squamous cell carcinoma (OSCC) and analyze the association between these factors and genesis and metastasis of OSCC. METHODS: The express of TGF-beta1, TbetaRI, TbetaRII and Smad4, a pivotal downstream molecule of its signaling, in 10 normal oral mucosa tissues and 108 OSCC was detected by SP immunohistochemistry, and thier correlation with genesis and metastasis of OSCC were assessed. RESULTS: The expressions of TbetaRII and Smad4 were lower in the tumors (34.3%, 38.9%) than those in the normal oral epithelium (80.0%, 100.0%, P < 0.05). The positive expression rates of TGF-beta1 and TbetaRI in the normal oral epithelium and OSCC were not significantly different (P > 0.05). There was an inverse correlation between TGF-beta1, Smad4, TbetaRII, TbetaRI expression and clinical stages (P < 0.01). The expression of TGF-beta1 was related with histological differentiation and tumor localization (P < 0.05). There was a relationship beteween Smad4 expression and histological differentiation and lymph node metastasis (P < 0.05). The expression of TbetaRII in the samples with lymph node metastasis was less than that in the ones without lymph node metastasis (P < 0.01), although there was no association between expression of TbetaRII and lymph node metastasis status. CONCLUSION: There is an important relationship between the abnormal TGF-beta1/Smad4 signal pathway and genesis and development of OSCC, while the low expressed Smad4 and TbetaRII may promote the metastasis of OSCC.


Assuntos
Carcinoma de Células Escamosas/metabolismo , Neoplasias Bucais/metabolismo , Transdução de Sinais , Fator de Crescimento Transformador beta1/metabolismo , Carcinoma de Células Escamosas/patologia , Membrana Celular/metabolismo , Citoplasma/metabolismo , Feminino , Humanos , Metástase Linfática , Masculino , Pessoa de Meia-Idade , Neoplasias Bucais/patologia , Estadiamento de Neoplasias , Proteínas Serina-Treonina Quinases/metabolismo , Receptor do Fator de Crescimento Transformador beta Tipo I , Receptor do Fator de Crescimento Transformador beta Tipo II , Receptores de Fatores de Crescimento Transformadores beta/metabolismo , Proteína Smad4/metabolismo
4.
Environ Sci Pollut Res Int ; 20(8): 5449-60, 2013 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-23430734

RESUMO

This work aims to analyze the relationship between root growth, mitogen-activated protein kinase (MAPK), auxin signaling, and cell cycle-related gene expression in cadmium (Cd)-stressed rice. The role of MAPKs in auxin signal modification and cell cycle-related gene expression during root growth was investigated by disrupting MAPK signaling using the MAPKK inhibitor PD98059 (PD). Treatment with Cd caused a significant accumulation of Cd in the roots. A Cd-specific probe showed that Cd is mainly localized in the meristematic zone and vascular tissues. Perturbation of MAPK signaling using PD significantly suppressed root system growth under Cd stress. The transcription of six MAPK genes was inhibited by Cd compared to the control. Detection using DR5-GUS transgenic rice showed that the intensity and distribution pattern of GUS staining was similar in roots treated with PD or Cd, whereas in Cd plus PD-treated roots, the GUS staining pattern was similar to that of the control, which indicates a close association of MAPK signaling with auxin homeostasis under control and Cd stress conditions. The expression of most key genes of auxin signaling, including OsYUCCA, OsPIN, OsARF, and OsIAA, and of most cell cycle-related genes, was negatively regulated by MAPKs under Cd stress. These results suggest that the MAPK pathway plays specific roles in auxin signal transduction and in the control of the cell cycle in response to Cd stress. Altogether, MAPKs take part in the regulation of root growth via auxin signal variation and the modified expression of cell cycle-related genes in Cd-stressed rice. A working model for the function of MAPKs in rice root systems grown under Cd stress is proposed.


Assuntos
Cádmio/toxicidade , Regulação da Expressão Gênica de Plantas/fisiologia , Genes cdc/genética , Ácidos Indolacéticos/metabolismo , Proteínas Quinases Ativadas por Mitógeno/metabolismo , Oryza/crescimento & desenvolvimento , Flavonoides/farmacologia , Genes de Plantas/genética , Proteínas Quinases Ativadas por Mitógeno/antagonistas & inibidores , Oryza/efeitos dos fármacos , Oryza/metabolismo , Raízes de Plantas/efeitos dos fármacos , Raízes de Plantas/crescimento & desenvolvimento , Raízes de Plantas/metabolismo , Brotos de Planta/efeitos dos fármacos , Brotos de Planta/crescimento & desenvolvimento , Inibidores de Proteínas Quinases/farmacologia , Transdução de Sinais
5.
Zhonghua Kou Qiang Yi Xue Za Zhi ; 45(7): 421-5, 2010 Jul.
Artigo em Chinês | MEDLINE | ID: mdl-21122435

RESUMO

OBJECTIVE: To investigate the inhibitory effect of transforming growth factor (TGF)-ß1 on oral squamous cell carcinoma (OSCC) Tb cell line. METHODS: Cell counting method was used to examine the inhibitory effect of TGF-ß1 on Tb cell and flow cytometry (FCM) assay performed to measure the changes of cell cycle. Superarray was used to screen the changing expression of genes in TGF-ß1/Smads signaling pathway.RT-PCR method was used to detect the results of Superarray. RESULTS: TGF-ß1 showed significant inhibiting effect on OSCC Tb cell line. TGF-ß1 blocked the cell cycle at G1 phase. The expression level of activin receptor-like kinase-1 (ACVRL-1), anti-mullerian hirmine (AMH), cyclim-dependent kinase inhibitor-2B (CDKN-2B) and transforming growth factor-beta-indnced factor (TGIF) was higer in the cells treated with TGF-ß1 than in control, while TDGF-1 expression was down-regulated. ACVRL-1 and CDKN-2B gene expression was consistent with the results of Superarray. CONCLUSIONS: TGF-ß1 can inhibit the growth of OSCC Tb cell line. The mechanism may be related to the regulation of cell cycle and the expression of ACVRL-1 and CDKN-2B in TGF-ß1-Smads signaling pathway.


Assuntos
Carcinoma de Células Escamosas/patologia , Fator de Crescimento Transformador beta1/farmacologia , Receptores de Activinas Tipo II/metabolismo , Hormônio Antimülleriano/metabolismo , Pontos de Checagem do Ciclo Celular , Linhagem Celular Tumoral , Inibidor de Quinase Dependente de Ciclina p15/metabolismo , Humanos , Metástase Neoplásica , Transdução de Sinais
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