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1.
J Fish Dis ; 44(3): 249-262, 2021 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-33314157

RESUMO

Takifugu rubripes and Dicentrarchus labrax are important commercial fish in China that are under serious threat from Cryptocaryon irritans. C. irritans is a ciliated obligate parasite that causes marine white spot disease and leads to heavy economic losses. We analysed the transcriptome in the gills of T. rubripes and D. labrax to compare differentially expressed genes (DEGs) and pathways during infection with C. irritans. In total, we identified 6,901 and 35,736 DEGs from T. rubripes and D. labrax, respectively. All DEGs were annotated into GO terms; 6,901 DEGs from T. rubripes were assigned into 991 sub-categories, and 35,736 DEGs from D. labrax were assigned into 8,517 sub-categories. We mapped DEGs to the KEGG database and obtained 153 and 350 KEGG signalling pathways from T. rubripes and D. labrax, respectively. Immune-related categories included Toll-like receptors, MAPK, lysosome, C-type lectin receptor and NOD-like receptor signalling pathways were significantly enriched pathways. In immune-related signalling pathways, we found that AP-1, P38, IL-1ß, HSP90 and PLA were significantly up-regulated DEGs in T. rubripes, but P38 and PLA were significantly down-regulated in D. labrax. In this study, transcriptome was used to analyse the difference between scaly and non-scaly fish infection by C. irritans, which not only provided a theoretical basis for the infection mechanism of C. irritans, but also laid a foundation for effectively inhibiting the occurrence of this disease. Our work provides further insight into the immune response of host resistance to C. irritans.

2.
J Formos Med Assoc ; 119(1 Pt 2): 319-326, 2020 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-31204145

RESUMO

PURPOSE: To compare the effect of unloading knee brace with physical therapy (PT) in Asian patients with osteoarthritis (OA) of the knee. METHOD: This is a non-random, two-group comparative study. Patients with medial compartment knee OA (n = 41) were assigned to either the brace group (n = 20) or PT group (n = 21). Patients in the brace group were fitted with an unloading knee brace for three months and the PT group received a 60-min session of physiotherapy over the affected knee, three times a week, for three months. The primary outcome measures were the pain visual analogue scale (VAS) and the Western Ontario McMaster University Osteoarthritis Index (WOMAC); the second outcome measures were the 36-item Short-Form Health Survey (SF-36) and patient's satisfaction. The patients were evaluated at baseline, and at one month and three months. RESULTS: Group comparison showed no significant difference regarding pain VAS, WOMAC, SF-36, and patient's satisfaction, except stiffness in WOMAC (P = .006) and social functioning in SF-36 (P = .007). Time and group interaction revealed significant differences only in general health (P = .007) and mental health (P = .006) of SF-36. Within-group comparison found that pain VAS and WOMAC decreased significantly at one months and three months in both groups. CONCLUSION: The effect of brace fitting in patients with knee OA was similar to that of physical therapy. A Western-made unloading knee brace is acceptable in some Asian people with knee OA. CLINICAL TRIAL REGISTRATION NUMBER: NCT02712710.


Assuntos
Braquetes , Osteoartrite do Joelho/fisiopatologia , Osteoartrite do Joelho/terapia , Modalidades de Fisioterapia , Idoso , Feminino , Humanos , Articulação do Joelho/fisiopatologia , Masculino , Pessoa de Meia-Idade , Medição da Dor , Amplitude de Movimento Articular , Taiwan , Escala Visual Analógica
3.
Int J Mol Sci ; 20(9)2019 May 03.
Artigo em Inglês | MEDLINE | ID: mdl-31058839

RESUMO

Given advancements in cancer immunity, cancer treatment has gained breakthrough developments. Immune checkpoint inhibitors, such as programmed cell death 1 (PD-1) inhibitors, are the most promising drugs in the field and have been approved to treat various types of cancer, such as metastatic melanoma, head and neck squamous cell carcinoma, and urothelial carcinoma. However, whether PD-1 inhibitors should be administered to renal transplant patients with advanced cancer remains unclear because the T-cells produced after administration of these inhibitors act against not only tumor antigens but also donor alloantigens. Thus, the use of PD-1 inhibitors in kidney-transplanted patients with advanced cancer is limited on account of the high risk of graft failure due to acute rejection. Hence, finding optimal treatment regimens to enhance the tumor-specific T-cell response and decrease T-cell-mediated alloreactivity after administration of a PD-1 inhibitor is necessary. Thus far, no recommendations for the use of PD-1 inhibitors to treat cancer in renal transplant patients are yet available, and very few cases reporting kidney-transplanted patients treated with PD-1 inhibitors are available in the literature. Therefore, in this work, we review the published cases and suggest feasible approaches for renal transplant patients with advanced malignancy treated by a PD-1 inhibitor. Of the 22 cases we obtained, four patients maintained intact grafts without tumor progression after treatment with a PD-1 inhibitor. Among these patients, one maintained steroid dose before initiation of anti-PD1, two received immunosuppressive regimens with low-dose steroid and calcineurin inhibitor (CNI)-elimination with sirolimus before initiation of anti-PD-1 therapy, and one received combined anti-PD-1, anti-vascular endothelial growth factor (VEGF), and chemotherapy with unchanged immunosuppressive regimens. mammalian target of rapamycin (mTOR) inhibitors and anti-VEGF may act as regulators of tumor-specific and allogenic T-cells. However, more studies are necessary to explore the optimal therapy and ensure the safety and efficacy of PD-1 inhibitors in kidney-transplanted patients.


Assuntos
Antineoplásicos Imunológicos/uso terapêutico , Transplante de Rim , Neoplasias/tratamento farmacológico , Receptor de Morte Celular Programada 1/antagonistas & inibidores , Animais , Antineoplásicos Imunológicos/farmacologia , Rejeição de Enxerto/imunologia , Humanos , Imunossupressores/farmacologia , Imunossupressores/uso terapêutico , Estadiamento de Neoplasias , Neoplasias/imunologia , Neoplasias/metabolismo , Neoplasias/patologia , Resultado do Tratamento
4.
Medicine (Baltimore) ; 97(45): e12829, 2018 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-30407283

RESUMO

This study assessed the effectiveness and safety of Chinese herbal medicine Ping Chuan Ke Li (PCKL) for the treatment of patients with mild/ moderate persistent asthma.A total of 108 eligible patients with persistent asthma were included and were divided into a treatment group and a control group in this retrospective study. All 108 patients underwent oral montelukast. Additionally, subjects in the treatment group also received PCKL therapy. All patients in both groups were treated for a total of 1 month. The primary outcome of lung function was evaluated by the forced expiratory volume in one second (FEV1) and FEV1/forced vital capacity (FVC). The secondary outcome of quality of life was assessed by St. George's Respiratory Questionnaire (SGRQ). Moreover, adverse events (AEs) were also recorded in this study. All outcome measurements were assessed after 1-month treatment.After 1-month treatment, patients in the treatment group did not demonstrate better outcome in the improvement of lung function, measured by FEV1 (P =.57, table 2), and FEV1/FVC (P =.29); and enhancement of quality of life, measured by SGRQ scale (total, P =.37; symptom, P =.32; activity, P =.39; impact, P =.83). In addition, no AEs differ between 2 groups.The results of this study showed that Chinese herbal PCKL may not benefit for patients with mild/moderate persistent asthma after 1-month treatment.


Assuntos
Asma/tratamento farmacológico , Medicamentos de Ervas Chinesas/uso terapêutico , Adulto , Feminino , Volume Expiratório Forçado/efeitos dos fármacos , Humanos , Masculino , Pessoa de Meia-Idade , Qualidade de Vida , Estudos Retrospectivos , Inquéritos e Questionários , Resultado do Tratamento , Capacidade Vital/efeitos dos fármacos
5.
Am J Phys Med Rehabil ; 97(2): 83-89, 2018 02.
Artigo em Inglês | MEDLINE | ID: mdl-28816704

RESUMO

OBJECTIVE: The aim of the study was to compare the effects of corticosteroid injection with lidocaine injection in treating tennis elbow. DESIGN: It is a prospective, double-blinded, randomized controlled trial. Patients with tennis elbow for more than 1 mo were recruited from a hospital-based rehabilitation outpatient clinic. A total of 70 patients were recruited, and 61 patients completed the study. Patients received an injection of either 10 mg (1 ml) of triamcinolone (corticosteroid group, n = 30) or 1 ml of 1% lidocaine (lidocaine group, n = 31). All of the outcome measures were evaluated before the intervention and at 2 wks and 2 mos after treatment. RESULTS: No significant group differences were observed between the corticosteroid and lidocaine groups regarding Patient-Rated Tennis Elbow Evaluation, Disability of the Arm, Shoulder, and Hand, visual analog scale for pain, and grip strength at baseline and at 2 wks and 2 mos after treatment (P > 0.05). However, within-group comparison showed significant improvement after injection with regard to Patient-Rated Tennis Elbow Evaluation, Disability of the Arm, Shoulder, and Hand, visual analog scale for pain, and grip strength in both groups (P > 0.05). CONCLUSIONS: No differences in the short-term outcomes were found between lidocaine and corticosteroid injection in a small sample of people with tennis elbow with mean duration of 3.8 mos.


Assuntos
Corticosteroides/administração & dosagem , Lidocaína/administração & dosagem , Cotovelo de Tenista/tratamento farmacológico , Adulto , Idoso , Método Duplo-Cego , Feminino , Força da Mão , Humanos , Injeções Intra-Articulares , Masculino , Pessoa de Meia-Idade , Medição da Dor , Estudos Prospectivos , Cotovelo de Tenista/fisiopatologia , Resultado do Tratamento
6.
J Thorac Dis ; 9(7): 2054-2060, 2017 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-28840006

RESUMO

BACKGROUND: Protein regulator of cytokinesis-1 (PRC1) has been shown to participate in the completion of cytokinesis, and it is dysregulated in cancer processes. However, its relevance in lung squamous cell carcinoma (SCC) remained largely unknown. We aimed to study the expression pattern of PRC1 and assess its clinical significance in lung SCC. METHODS: PRC1 protein expression in human lung SCC and adjacent normal lung tissues was detected by immunohistochemistry. PRC1 expression was assessed in association with clinicopathological features and clinical outcomes of lung SCC patients. RESULTS: In lung SCC tissues, PRC1 protein expression was significantly higher than those in paired normal lung tissues. The lung SCC patients with PRC1 overexpression had an advanced pathological stage (TNM stage), positive lymph node metastasis, and a shorter overall survival (OS) time more frequently than patients with low PRC1 expression. Additional, PRC1 expression was also shown to be poor as a prognostic factor for OS in patients with lung SCC. CONCLUSIONS: Our study indicated that aberrant expression of PRC1 may point to biochemical recurrence in lung SCC. This highlights its potential as a valuable prognostic marker for lung SCC.

7.
Mol Cancer ; 16(1): 108, 2017 06 24.
Artigo em Inglês | MEDLINE | ID: mdl-28646916

RESUMO

BACKGROUND: Protein regulator of cytokinesis-1 (PRC1) belongs to the microtubule-associated proteins (MAPs) family, and is involved in cytokinesis. Recent investigations suggest PRC1 involvement in human carcinogenesis, including breast carcinoma, hepatocellular carcinoma and etc. However, whether PRC1 contributes to lung adenocarcinoma tumorigenesis remains unknown. METHODS: Quantitative reverse-transcription polymerase chain reaction (qRT-PCR), Western blotting and Immunohistochemical staining (IHC) were used to evaluate and contrast the PRC1 expression profile in lung adenocarcinoma and adjacent normal lung tissues. We examined the clinical use of PRC1 in lung adenocarcinoma prognosis. Additionally, the tumorigenesis impact of PRC1 in lung adenocarcinoma cells was verified via in vitro and in vivo metastasis and tumorigenesis assays. Notably, Next Generation Sequencing (NGS) was performed to investigate the molecular mechanism underlying the oncogenic role of PRC1 in lung adenocarcinoma. RESULTS: PRC1 mRNA and protein expressions were upregulated in lung adenocarcinoma tissues compared to adjacent normal lung tissues. PRC1 protein overexpression correlated with lymph node metastasis and was an independent poor prognostic factor for lung adenocarcinoma patients. Our data implied that PRC1 depletion limited the proliferation and invasion of lung adenocarcinoma cells in vitro and lowered tumor development and lung metastasis in vivo. Remarkably, limiting PRC1 substantially prompted G2/M phase cell cycle arrest and apoptosis. Mechanistically, by conducting NGS on PRC1-depleted A549 cells and control cells, we discovered that PRC1 expression was significantly correlated with the Wnt signaling pathway. CONCLUSIONS: This investigation offers confirmation that PRC1 is a prognostic and promising therapeutic biomarker for people with lung adenocarcinoma and takes on a key part in the activation of the Wnt/ß-catenin pathway in lung adenocarcinoma development.


Assuntos
Adenocarcinoma/mortalidade , Adenocarcinoma/patologia , Proteínas de Ciclo Celular/genética , Proteínas de Ciclo Celular/metabolismo , Neoplasias Pulmonares/mortalidade , Neoplasias Pulmonares/patologia , Via de Sinalização Wnt/fisiologia , Adenocarcinoma/genética , Adenocarcinoma/metabolismo , Adenocarcinoma de Pulmão , Idoso , Animais , Apoptose/genética , Linhagem Celular Tumoral , Feminino , Pontos de Checagem da Fase G2 do Ciclo Celular/genética , Regulação Neoplásica da Expressão Gênica , Sequenciamento de Nucleotídeos em Larga Escala , Humanos , Neoplasias Pulmonares/genética , Neoplasias Pulmonares/metabolismo , Masculino , Camundongos Endogâmicos BALB C , Pessoa de Meia-Idade , Prognóstico , Ensaios Antitumorais Modelo de Xenoenxerto , beta Catenina/genética , beta Catenina/metabolismo
8.
Transl Lung Cancer Res ; 6(1): 23-34, 2017 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-28331821

RESUMO

BACKGROUND: With the release of the National Lung Screening Trial results, the detection of peripheral pulmonary lesions (PPLs) is likely to increase. Computed tomography (CT)-guided percutaneous transthoracic needle biopsy (PTNB) and radial probe endobronchial ultrasound (r-EBUS)-guided transbronchial lung biopsy (TBLB) are recommended for tissue diagnosis of PPLs. METHODS: A systematic review of published literature evaluating the accuracy of r-EBUS-TBLB and CT-PTNB for the diagnosis of PPLs was performed to determine point sensitivity and specificity, and to construct a summary receiver-operating characteristic curve. RESULTS: This review included 31 publications dealing with EBUS-TBLB and 14 publications dealing with CT-PTNB for the diagnosis of PPLs. EBUS-TBLB had point sensitivity of 0.69 (95% CI: 0.67-0.71) for the diagnosis of peripheral lung cancer (PLC), which was lower than the sensitivity of CT-PTNB (0.94, 95% CI: 0.94-0.95). However, the complication rates observed with EBUS-TBLB were lower than those reported for CT-PTNB. CONCLUSIONS: This meta-analysis showed that EBUS-TBLB is a safe and relatively accurate tool in the investigation of PLC. Although the yield remains lower than that of CT-PTNB, the procedural risks are lower.

9.
PeerJ ; 5: e3003, 2017.
Artigo em Inglês | MEDLINE | ID: mdl-28229027

RESUMO

BACKGROUND: Colorectal cancer (CRC) is one of the leading cancers worldwide. Several studies have performed microarray data analyses for cancer classification and prognostic analyses. Microarray assays also enable the identification of gene signatures for molecular characterization and treatment prediction. OBJECTIVE: Microarray gene expression data from the online Gene Expression Omnibus (GEO) database were used to to distinguish colorectal cancer from normal colon tissue samples. METHODS: We collected microarray data from the GEO database to establish colorectal cancer microarray gene expression datasets for a combined analysis. Using the Prediction Analysis for Microarrays (PAM) method and the GSEA MSigDB resource, we analyzed the 14,698 genes that were identified through an examination of their expression values between normal and tumor tissues. RESULTS: Ten genes (ABCG2, AQP8, SPIB, CA7, CLDN8, SCNN1B, SLC30A10, CD177, PADI2, and TGFBI) were found to be good indicators of the candidate genes that correlate with CRC. From these selected genes, an average of six significant genes were obtained using the PAM method, with an accuracy rate of 95%. The results demonstrate the potential of utilizing a model with the PAM method for data mining. After a detailed review of the published reports, the results confirmed that the screened candidate genes are good indicators for cancer risk analysis using the PAM method. CONCLUSIONS: Six genes were selected with 95% accuracy to effectively classify normal and colorectal cancer tissues. We hope that these results will provide the basis for new research projects in clinical practice that aim to rapidly assess colorectal cancer risk using microarray gene expression analysis.

10.
J Cell Mol Med ; 21(4): 665-676, 2017 04.
Artigo em Inglês | MEDLINE | ID: mdl-27862966

RESUMO

NCAPG2 is a component of the condensin II complex and contributes to chromosome segregation via microtubule-kinetochore attachment during mitosis. It is well known that NCAPG2 plays a critical role in cell mitosis; however, the role of altered NCAPG2 expression and its transcriptional regulatory function in cancer development remains mostly unknown. Here, for the first time we reported that NCAPG2 was evidently increased in non-small cell lung cancer tissues compared to adjacent normal lung tissues. Clinicopathological data analysis showed that NCAPG2 overexpression was significantly correlated with lymph node metastasis and pathologic-Tumour Nodes Metastasen stages, and was an independent prognostic factor in lung adenocarcinoma patients. Moreover, siRNA-mediated knockdown of NCAPG2 could inhibit tumour cell growth of lung adenocarcinoma cells (A549 and H1299) in vitro and could significantly lead to cell cycle arrest in the G2 phase. Furthermore, we found that NCAPG2 silencing significantly decreased the expression levels of G2/M phase cell cycle-related protein expressions (Cyclin B1, Cdc2) and increased the expression levels of p27 and p21 through Western blot analysis. Taken together, we demonstrated that increased NCAPG2 expression could regulate cell proliferation and identified as a poor prognostic biomarker in lung adenocarcinoma.


Assuntos
Adenocarcinoma/genética , Adenocarcinoma/patologia , Proteínas Cromossômicas não Histona/genética , Fase G2 , Neoplasias Pulmonares/genética , Neoplasias Pulmonares/patologia , Mitose , Adenocarcinoma de Pulmão , Idoso , Pontos de Checagem do Ciclo Celular/genética , Proteínas de Ciclo Celular/metabolismo , Linhagem Celular Tumoral , Proliferação de Células , Proteínas Cromossômicas não Histona/metabolismo , Feminino , Regulação Neoplásica da Expressão Gênica , Técnicas de Silenciamento de Genes , Inativação Gênica , Humanos , Masculino , Análise Multivariada , Prognóstico , Proteínas Serina-Treonina Quinases/metabolismo , Proteínas Proto-Oncogênicas/metabolismo , RNA Interferente Pequeno/metabolismo , Análise de Sobrevida , Regulação para Cima/genética
11.
Tumour Biol ; 2016 Oct 22.
Artigo em Inglês | MEDLINE | ID: mdl-27771855

RESUMO

Malignant pleural effusion (MPE) is associated with a poor prognosis in lung cancer. Currently, no effective cure exists for MPE. Chloroquine (CQ) has been demonstrated to induce vascular normalization and inhibit tumor growth. The aim of this study was to assess whether CQ affects MPE. The xenografts mice were divided into normal saline (NS), CQ, or bevacizumab (BE) group. Tumor growth and microvascular density (MVD) were monitored. We explored the effect of CQ on the proliferation, survival, and proangiogenic signaling of tumor cells in vitro. We further evaluated the effects of CQ on the viability, migration, and tube formation of human umbilical vein endothelial cells (HUVECs). A chicken chorioallantoic membrane (CAM) model was used to elucidate the effects of CQ on angiogenesis. Finally, an MPE mouse model were treated by CQ, BE, or NS. The volume of pleural effusion, tumor foci, and MVD was evaluated. CQ therapy group exhibited decreased tumor volume, tumor weight, and MVD in the mouse xenografts. CQ inhibited the proliferation of the tumor cells. However, the expression of vascular endothelial growth factor was not affected. Additionally, CQ inhibited the proliferation, migration, and tube formation of HUVECs and also restrained angiogenesis in the CAM. Western blot showed that CQ might suppress angiogenesis by downregulating p-Akt, Jagged1, and Ang2 in HUVECs. In MPE mice, the volume of the pleural effusion, the number of pleural tumor foci, and the MVD were significantly reduced in the CQ group. Our work demonstrated that CQ played the role of an efficient treatment for MPE.

12.
Biomed Res Int ; 2015: 745410, 2015.
Artigo em Inglês | MEDLINE | ID: mdl-26295050

RESUMO

BACKGROUND: Neck circumference (NC) is an anthropometric measure of obesity for upper subcutaneous adipose tissue distribution which is associated with cardiometabolic risk. This study investigated whether NC is associated with indicators of chronic kidney disease (CKD) for high cardiometabolic risk patients. METHODS: A total of 177 consecutive patients who underwent the outpatient departments of cardiology were prospectively enrolled in the study. The patients were aged >20 years with normal renal function or with stages 1-4 CKD. A linear regression was performed using the Enter method to present an unadjusted R(2), standardized coefficients, and standard error, and the Durbin-Watson test was used to assess residual independence. RESULTS: Most anthropometric measurements from patients aged ≧ 65 were lower than those from patients aged < 65, except for women's waist circumference (WC) and waist hip ratio. Female NC obtained the highest R(2) values for 24 hr CCR, uric acid, microalbuminuria, hsCRP, triglycerides, and HDL compared to BMI, WC, and hip circumference. The significances of female NC with 24 hr CCR and uric acid were improved after adjusted age and serum creatinine. CONCLUSIONS: NC is associated with indicators of CKD for high cardiometabolic risk patients and can be routinely measured as easy as WC in the future.


Assuntos
Doenças Cardiovasculares/epidemiologia , Pescoço/anatomia & histologia , Obesidade/epidemiologia , Insuficiência Renal Crônica/epidemiologia , Adulto , Idoso , Antropometria , Índice de Massa Corporal , Doenças Cardiovasculares/sangue , Doenças Cardiovasculares/fisiopatologia , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Obesidade/sangue , Obesidade/fisiopatologia , Insuficiência Renal Crônica/sangue , Insuficiência Renal Crônica/fisiopatologia , Fatores de Risco , Triglicerídeos/sangue , Circunferência da Cintura
13.
Chin Med J (Engl) ; 126(18): 3539-44, 2013.
Artigo em Inglês | MEDLINE | ID: mdl-24034105

RESUMO

BACKGROUND: Claudin-6 is a protein component of tight junctions and its expression could downregulate the malignant phenotype of breast carcinoma. Here we investigated the mechanisms of claudin-6 induced human MCF-7 breast cancer cells apoptosis, invasion, and migration. METHODS: Terminal deoxyribonucleotide transferase-mediated nick-end labeling assay and Annexin-V/PI double stain assay were carried out to evaluate apoptosis. Inhibitors of each pathway were used to inactivate the signaling pathways. The expression of claudin-6 and phosphate p38, Erk 1/2 and Akt protein levels was confirmed by Western blotting analysis. Invasive and migratory traits of claudin-6 expressing cells were determined by Boyden chamber invasion assay and monolayer wound-healing assay. RESULTS: Cells with high-level expression of claudin-6 had a higher rate of apoptosis than control cells. Western blotting assay showed that by contrast to control groups, p38 pathways were more activated in claudin-6 expressing cells. However, after inhibitor SB203580 treatment, the activation status could be significantly counteracted. Furthermore, by applying inhibitors to the apoptotic rate, invasive and migratory traits were also recovered in cells with claudin-6 expression. CONCLUSION: Claudin-6 may function through p38 mitogen-activated protein kinase pathway, of which inhibition may reverse claudin-6-induced cell apoptosis, invasion, and migration.


Assuntos
Apoptose/fisiologia , Movimento Celular/fisiologia , Claudinas/metabolismo , Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo , Apoptose/genética , Western Blotting , Movimento Celular/genética , Claudinas/genética , Humanos , Marcação In Situ das Extremidades Cortadas , Sistema de Sinalização das MAP Quinases/genética , Sistema de Sinalização das MAP Quinases/fisiologia , Células MCF-7 , Proteínas Quinases p38 Ativadas por Mitógeno/genética
14.
Zhonghua Bing Li Xue Za Zhi ; 39(1): 44-7, 2010 Jan.
Artigo em Chinês | MEDLINE | ID: mdl-20388399

RESUMO

OBJECTIVE: To explore the role of estrogen in the regulation of the expression of claudin-6 and biological behavior in MCF-7 cells. METHODS: RT-PCR and immunocytochemistry were conducted to analyze the expression and localization of claudin-6 in MCF-7 cells treated with 17ß-estradiol. CCK-8 kit assay and Scratch Test were conducted to analyze the capability of proliferation and migration of 17ß-estradiol treated MCF-7 cells. RESULTS: RT-PCR analysis and immunocytochemistry showed that 17ß-estradiol induced a concentration-and time-dependent effect on claudin-6. At 5 nmol/L and at 24 h, 17ß-estradiol treatment led to an increased level of claudin-6, which was located in the membrane of MCF-7 cells. CCK-8 analysis showed a significant decrease in the capability of proliferation of MCF-7 cells compared with the control group (P < 0.05). Cells Scratch Test showed decreased migration capability of MCF-7 cells compared with the control group (P > 0.05). CONCLUSIONS: 17ß-E2 might regulate the expression of claudin-6 and inhibit the proliferation and migration of MCF-7 cells. The inhibitory effects of 17ß-E2 on growth and migration of MCF-7 cells may be mediated by claudin-6 expression regulation.


Assuntos
Neoplasias da Mama/patologia , Movimento Celular/efeitos dos fármacos , Proliferação de Células/efeitos dos fármacos , Estradiol/farmacologia , Proteínas de Membrana/metabolismo , Neoplasias da Mama/metabolismo , Linhagem Celular Tumoral , Claudinas , Relação Dose-Resposta a Droga , Estradiol/administração & dosagem , Feminino , Humanos
15.
Zhonghua Yi Xue Za Zhi ; 90(6): 407-12, 2010 Feb 09.
Artigo em Chinês | MEDLINE | ID: mdl-20367941

RESUMO

OBJECTIVE: To explore the effect of over-expression of tight junction protein claudin-6 upon the biological characters of breast cancer cell line MCF-7. METHODS: The MCF-7 subline expressing a high level of claudin-6 was established by transfection with a pcDNA3.1-claudin-6 expression vector. The expression of claudin-6 in mRNA and its protein level were confirmed by RT-PCR, Western blot and immunofluorescent assays. Then the effect of claudin-6 upon cell proliferation was examined by MTT assay. Colony-forming assays were used to examine 2-D and 3-D colony-forming capacities. Invasive and migratory traits of claudin-6 expressing cells were determined by Boyden chamber invasion assay and monolayer wound-healing assay. The structure and function of tight junctions in both parental and claudin-6 expression MCF-7 cells were evaluated by measuring transepithelial electrical resistance. RESULTS: Immunofluorescent assays showed that transfected cells expressed claudin-6 on their membrane. Cells with a high level expression of claudin-6 grew slowly than control cells. Anchorage-independent growth, invasive and migratory traits also decreased substantially in cells with claudin-6 expression; whereas the transepithelial electrical resistance increased in the claudin-6 transfected cells. CONCLUSION: The up-regulation of claudin-6 expression in MCF-7 breast cancer cells suppresses their malignant phenotypes with a correlation with the restoration of tight junction integrity. Claudin-6 may function as a cancer suppressor whose down-regulation contributes to the malignant progression of certain types of breast cancers.


Assuntos
Neoplasias da Mama/metabolismo , Proteínas de Membrana/metabolismo , Junções Íntimas/metabolismo , Neoplasias da Mama/patologia , Linhagem Celular Tumoral , Claudinas , Regulação para Baixo , Feminino , Humanos , Invasividade Neoplásica , Junções Íntimas/patologia , Transfecção
16.
Environ Microbiol ; 9(3): 819-23, 2007 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-17298380

RESUMO

Avoparcin, a vancomycin analogue, was banned as a feed additive in Taiwan in 2000. A nationwide surveillance was conducted to study the prevalence of vancomycin-resistant enterococci (VRE) on chicken farms between 2000 and 2003. Among the 1021 E. faecalis and 967 E. faecium isolates studied, resistance to tetracycline, erythromycin, high-level aminoglycosides, ciprofloxacin and chloramphenicol either increased or remained high except vancomycin. The proportion of VRE decreased, between 2000 and 2003, from 13.7% (22/161) to 3.7% (11/299) for E. faecalis, and 3.4% (4/119) to 0% (0/300) for E. faecium. Only 8.8% (7/80) of the chicken farms surveyed harboured VRE in 2003 compared with 25% (15/60) in 2000. All VRE were resistant to tetracycline and erythromycin. All VRE possess the vanA gene but nearly all (79 of 83 isolates) were susceptible to teicoplanin, indicating VanB phenotype. Some clones were detected from different farms in various regions over the years. We conclude that the frequency of VRE in chicken farms decreased in association with a ban on avoparcin; and the continued presence of VRE may be due to the ability of some strains to persist in the farms, transfer of vancomycin resistance determinants or co-selection by the continued use of other antibiotics.


Assuntos
Criação de Animais Domésticos , Galinhas/microbiologia , Enterococcus faecalis/isolamento & purificação , Enterococcus faecium/isolamento & purificação , Resistência a Vancomicina , Animais , Antibacterianos/farmacologia , Proteínas de Bactérias/genética , Carbono-Oxigênio Ligases/genética , Enterococcus faecalis/efeitos dos fármacos , Enterococcus faecalis/genética , Enterococcus faecium/efeitos dos fármacos , Enterococcus faecium/genética , Glicopeptídeos , Testes de Sensibilidade Microbiana , Taiwan , Resistência a Vancomicina/genética
17.
J Neurochem ; 93(4): 1010-20, 2005 May.
Artigo em Inglês | MEDLINE | ID: mdl-15857404

RESUMO

Gulf war illnesses (GWI) are currently affecting thousands of veterans. To date, the molecular mechanisms underlying the pathogenesis of these illnesses remain unknown. During Gulf war I, military personnel were exposed to multiple stressors, one or more vaccines, pyridostigmine (PY), and other chemicals. In our previous studies, we found that stress induces activation of mitogen activated protein-kinase kinase 4 (MKK4) and c-Jun-N-terminal kinase (JNK) in the mouse brain (Liu et al. 2004). Our working hypothesis is that stress, vaccination, and PY may synergistically induce activation of MKK4 and JNK in the brain, leading to over-activation of these kinases and neurological injuries. To test our hypothesis, we examined the effect of keyhole limpet hemocyanin (KLH) immunization alone or in combination with PY on activation of MKK4 and JNK induced by stress. We found that KLH immunization alone had a small effect on MKK4 or JNK activity but it significantly enhanced and prolonged activation of these kinases induced by stress, from a few hours to several days. Additionally, KLH immunization caused activation of p38MAPK. PY treatment further enhanced and prolonged activation of these kinases induced by stress in combination with KLH immunization and triggered activation of caspase-3. Our current studies suggest that stress, vaccination, and PY may synergistically act on multiple stress-activated kinases in the brain to cause neurological impairments in GWI.


Assuntos
Encéfalo/efeitos dos fármacos , Proteínas Quinases JNK Ativadas por Mitógeno/metabolismo , Proteína Quinase 13 Ativada por Mitógeno/metabolismo , Brometo de Piridostigmina/farmacologia , Estresse Fisiológico/enzimologia , Vacinação , Animais , Comportamento Animal/efeitos dos fármacos , Encéfalo/anatomia & histologia , Encéfalo/enzimologia , Caspase 3 , Caspases/metabolismo , Inibidores da Colinesterase/farmacologia , Sinergismo Farmacológico , Ativação Enzimática/efeitos dos fármacos , Ativação Enzimática/fisiologia , Hemocianinas/farmacologia , Imuno-Histoquímica/métodos , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Natação , Fatores de Tempo , Vacinação/métodos , Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo
18.
J Neurochem ; 89(4): 1034-43, 2004 May.
Artigo em Inglês | MEDLINE | ID: mdl-15140201

RESUMO

Stress is a part of daily life. However, molecular mechanisms underlying the activation of limbic-hypothalamic-pituitary-adrenal (LHPA) axis remains unknown. In this study, we explored whether activation of the mitogen-activated kinase kinase 4 (MKK4)-c-Jun-N-terminal kinase (JNK) signaling pathway may play a role in the activation of the LHPA axis. We found that forced-swim stress induced elevation of activated MKK4 in the hippocampal formation, amygdala, and hypothalamus. Unlike MKK4, a high basal level of JNK activity is present in many brain areas of unstressed mice. Forced-swim stress significantly elevated JNK activity in the hypothalamus and amygdala and, to a lesser extent, in the cortex, CA1 and CA3 regions, and the dentate gyrus. To further investigate the role of MKK4 and JNK in induction of stress responses, we investigated whether a different stress, namely, restraint stress, induced activation of MKK4 or JNK in the brain. We found that restraint stress also induced elevation of activated MKK4 and JNK in the hippocampal formation, amygdala, and hypothalamus. Because MKK4 and JNK were activated within 5 min following stress, we propose that the MKK4-JNK signaling may be an early neural event in the initiation of neuroendocrine, autonomic and behavioral stress responses.


Assuntos
Encéfalo/enzimologia , MAP Quinase Quinase 4 , Quinases de Proteína Quinase Ativadas por Mitógeno/metabolismo , Proteínas Quinases Ativadas por Mitógeno/metabolismo , Estresse Fisiológico/enzimologia , Tonsila do Cerebelo/enzimologia , Animais , Tronco Encefálico/enzimologia , Giro Denteado/enzimologia , Ativação Enzimática/fisiologia , Hipotálamo/enzimologia , Proteínas Quinases JNK Ativadas por Mitógeno , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Lobo Parietal/enzimologia , Tálamo/enzimologia
19.
J Biol Chem ; 278(35): 33364-9, 2003 Aug 29.
Artigo em Inglês | MEDLINE | ID: mdl-12810713

RESUMO

In our previous studies, we found that expression of polyglutamine-expanded huntingtin in HN33 cells induced sensitization of N-methyl-D-aspartate (NMDA) receptors (Sun, Y., Savinainen, A., and Liu, Y. F. (2001) J. Biol. Chem. 276, 24713-24718). Following this study, we investigated whether tyrosine phosphorylation of NMDA receptors might contribute to the altered property of the receptors. Expression of polyglutamine-expanded huntingtin induced elevation of phosphorylated or activated Src and increased targeting of PSD-95 (post-synaptic density 95) and activated Src to cell surface membrane. Expression of the mutated huntingtin also induced tyrosine phosphorylation of NR2B (NMDA receptor 2B) subunits, and co-expression of PSD-95 enhanced the phosphorylation. Treatment of SU6656 (a specific Src inhibitor) or co-expression of a mutated NR2B subunit with mutations of all three major tyrosine phosphorylation sites significantly attenuated neuronal toxicity induced by the mutated huntingtin. Addition of AP-5 did not further inhibit the neuronal toxicity. Taken together, our studies show that polyglutamine-expanded huntingtin increases tyrosine phosphorylation of NMDA receptors via PSD-95 and Src, and increased tyrosine phosphorylation may contribute to the sensitization of the receptors mediated by polyglutamine-expanded huntingtin.


Assuntos
Proteínas do Tecido Nervoso/química , Proteínas Nucleares/química , Peptídeos/química , Receptores de N-Metil-D-Aspartato/química , Tirosina/metabolismo , Morte Celular , Linhagem Celular , Membrana Celular/metabolismo , Inibidores Enzimáticos/farmacologia , Humanos , Proteína Huntingtina , Imuno-Histoquímica , Marcação In Situ das Extremidades Cortadas , Microscopia de Fluorescência , Mutação , N-Metilaspartato/química , Fosforilação , Plasmídeos/metabolismo , Testes de Precipitina , Ligação Proteica , Receptores de N-Metil-D-Aspartato/metabolismo , Fatores de Tempo , Transfecção , Tirosina/química
20.
J Neurochem ; 83(4): 828-36, 2002 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-12421354

RESUMO

Based on the critical role of actin in the maintenance of synaptic function, we examined whether expression of familial beta-amyloid precursor protein APP-V642I (IAPP) or mutant presenilin-1 L286V (mPS1) affects actin polymerization in rat septal neuronal cells. Expression of either IAPP or mPS1 but not wild-type amyloid precursor protein or presenilin-1induced formation of actin stress fibers in SN1 cells, a septal neuronal cell line. Treatment with beta-amyloid (Abeta) peptide also caused formation of actin stress fibers in SN1 cells and primary cultured hippocampal neurons. Treatment with a gamma-secretase inhibitor completely blocked formation of actin stress fibers, indicating that overproduction of Abeta peptide induces actin stress fibers. Because activation of the p38 mitogen-activated protein kinase (p38MAPK)-mitogen-associated protein kinase-associated protein kinase (MAPKAPK)-2-heat-shock protein 27 signaling pathway mediates actin polymerization, we explored whether Abeta peptide activates p38MAPK and MAPKAPK-2. Expression of IAPP or mPS1 induced activation of p38MAPK and MAPKAPK-2. Treatment with a p38MAPK inhibitor completely inhibited formation of actin stress fibers mediated by Abeta peptide, IAPP or mPS1. Moreover, treatment with a gamma-secretase inhibitor completely blocked activation of p38MAPK and MAPKAPK-2. In summary, our data suggest that overproduction of Abeta peptide induces formation of actin stress fibers through activation of the p38MAPK signaling pathway in septal neuronal cells.


Assuntos
Peptídeos beta-Amiloides/farmacologia , Proteínas de Choque Térmico , Proteínas Quinases Ativadas por Mitógeno/metabolismo , Neurônios/efeitos dos fármacos , Neurônios/metabolismo , Fibras de Estresse/metabolismo , Actinas/metabolismo , Doença de Alzheimer/genética , Substituição de Aminoácidos , Secretases da Proteína Precursora do Amiloide , Peptídeos beta-Amiloides/genética , Precursor de Proteína beta-Amiloide/genética , Precursor de Proteína beta-Amiloide/farmacologia , Animais , Ácido Aspártico Endopeptidases , Linhagem Celular , Células Cultivadas , Endopeptidases/efeitos dos fármacos , Inibidores Enzimáticos/farmacologia , Proteínas de Choque Térmico HSP27 , Hipocampo/citologia , Peptídeos e Proteínas de Sinalização Intracelular , Proteínas de Membrana/genética , Proteínas de Membrana/farmacologia , Camundongos , Chaperonas Moleculares , Mutação , Proteínas de Neoplasias/metabolismo , Neurônios/citologia , Presenilina-1 , Proteínas Serina-Treonina Quinases/metabolismo , Ratos , Transdução de Sinais/fisiologia , Transfecção , Proteínas Quinases p38 Ativadas por Mitógeno
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