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3.
Sci Prog ; 104(2): 368504211011341, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-33881940

RESUMO

Apelin (APLN) is recently demonstrated a direct association with many malignant diseases. However, its effects on cervical cancer remain unclear. This study therefore aims to evaluate the association between APLN expression and cervical cancer using publicly available data from The Cancer Genome Atlas (TCGA). The Pearson χ2 test and Fish exact test, as well as logistic regression, were used to evaluate the relationship between clinicopathological factors in cervical cancer and the expression of APLN. Additionally, the Cox regression and Kaplan-Meier methods were conducted to analyze the Overall Survival (OS) of cervical cancer patients in TCGA. Finally, gene set enrichment analysis (GSEA) was performed to establish its biological functions. High expression of APLN in cervical cancer was significantly associated with a more advanced clinical stage (OR = 1.91 (1.21-3.05) for Stage II, Stage III, and Stage IV vs Stage I, p = 0.006). Additionally, it was associated with poor outcome after primary therapy (OR = 2.14 (1.03-4.59) for Progressive Disease (PD), Stable Disease (SD), and Partial Response (PR) vs Complete Remission (CR), p = 0.045) and high histologic grade (OR = 1.67 (1.03-2.72) for G3 and G4 vs G1 and G2, p = 0.037). Moreover, multivariate analysis showed that high expression of APLN was associated with a shorter OS. GSEA demonstrated that six KEGG pathways, including PPAR signaling, ECM-receptor interaction, focal adhesion, MAPK signaling, TGF-beta signaling, and Gap junction pathways were differentially enriched in the high expression APLN phenotype. The recent study suggests that APLN plays an important role in the progression of cervical cancer and might be a promising prognostic biomarker of the disease.

4.
J Ethnopharmacol ; 272: 113920, 2021 May 23.
Artigo em Inglês | MEDLINE | ID: mdl-33607200

RESUMO

ETHNOPHARMACOLOGICAL RELEVANCE: Pinoresinol diglucoside (PDG), the active compound extracted from Eucommia ulmoides, Styrax sp. and Forsythia suspensa, plays the roles in regulating hypertension, inflammation and oxidative stress. AIMS: Considering that hypertension and inflammation has been proved to contribute to cardiac remodeling, we tested the effects of PDG on cardiac hypertrophy (CM). METHODS: Male Sprague Dawley (SD) rats were used to construct hypertrophic rats by partial abdominal aortic constriction (AAC)-surgery. PDG solution (2 mg/ml) was used to treat AAC-induced rats by intraperitoneal injection at low dose (L-PDG, 2.5 mg/kg per day), medium dose (M-PDG, 5 mg/kg per day), and high dose (H-PDG, 7.5 mg/kg per day) for 3 weeks post AAC-surgery. CM was evaluated by the ratio of left ventricular weight to body weight ratio (LVW/BW), left ventricular wall thickness by H&E staining, and collagen content deposit by Masson's staining. Further, isoproterenol (ISO) and phenylephrine (PE) were used to produce cellular models of CM in neonatal rat ventricular cardiomyocytes (NRVMs). PDG pre-treated NRVMs 2 h at low dose (L-PDG, 2.5 µg/ml), medium dose (M-PDG, 5 µg/ml), and high dose (H-PDG, 7.5 µg/ml) for 24 h with or without PE- and ISO-stimulation. CM was evaluated by the expressions of hypertrophic biomarkers. Next, the hypertrophic biomarkers and pro-inflammatory cytokines were measured using quantitative real-time PCR (qRT-PCR), the expressions of protein kinase B (AKT)/mammalian target of rapamycin (mTOR)/transcription factor nuclear factor-kappa B (NF-kB) signaling pathway were determined by Western blotting. RESULTS: PDG treatment prevented cardiac histomorphology damages, decreased upregulations of hypertrophic biomarkers, and prevented fibrosis and inflammation after pressure overload resulting from AAC-surgery. Consistently, PDG remarkably inhibited the changes of cardiomyocyte hypertrophic biomarkers and inflammatory responses in cellular models of CM. Interestingly, PDG administration inhibited the activation of AKT/mTOR/NF-kB signaling pathway both in vivo and in vitro. CONCLUSIONS: PDG prevents AAC-induced CM in vivo, PE- and ISO-induced CM in vitro. The AKT/mTOR/NF-kB signaling pathway could be the potential therapeutic target involved in the protection of PDG. These findings provide novel evidence that PDG might be a promising therapeutic strategy for CM.


Assuntos
Cardiomegalia/tratamento farmacológico , Lignanas/farmacocinética , Lignanas/uso terapêutico , NF-kappa B/metabolismo , Proteínas Proto-Oncogênicas c-akt/metabolismo , Transdução de Sinais/efeitos dos fármacos , Serina-Treonina Quinases TOR/metabolismo , Animais , Animais Recém-Nascidos , Aorta Abdominal/cirurgia , Cardiomegalia/etiologia , Cardiomegalia/patologia , Constrição Patológica , Modelos Animais de Doenças , Fibrose/prevenção & controle , Inflamação/prevenção & controle , Isoproterenol/toxicidade , Masculino , Miócitos Cardíacos/efeitos dos fármacos , Fenilefrina/toxicidade , Pressão , Cultura Primária de Células , Ratos Sprague-Dawley , Remodelação Ventricular/efeitos dos fármacos
5.
Surg Endosc ; 35(7): 3421-3429, 2021 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-32661709

RESUMO

BACKGROUND AND AIMS: This study aimed to examine the fundamental characteristics of gastrointestinal (GI) endoscopy trials and evaluate their publication status. METHODS: A cross-sectional analysis was performed in the ClinicalTrials.gov database, and then the PubMed, Medline, Google Scholar, and Embase databases were searched. A dataset containing GI endoscopy clinical studies from ClinicalTrials.gov registered until November 24, 2017, was downloaded. Data of observational and interventional studies were extracted and analyzed. Publications in peer-reviewed journals were examined for completed trials, and factors associated with publication were identified. RESULTS: A total of 1338 of 253,777 clinical trials were assigned into GI endoscopy, of which 1018 were interventional and 320 were observational studies. Of all the trials, those from the USA comprised the largest percentage (n = 377, 28.18%). The most common field for registered trials was gastroscopy (n = 436, 32.6%), followed by colonoscopy (n = 215, 16.1%), endoscopic ultrasound (n = 186, 13.9%), endoscopic retrograde cholangiopancreatography (n = 176, 13.1%), and novel endoscopic procedure (n = 103, 7.7%). A total of 501 trials were completed before November 25, 2015, 281 (56.1%) of which were published. The median time from study completion to publication was 21 months (interquartile range, 12-32 months). Trials that were comprised of medium sample sizes (150-1000 subjects), conducted in Europe or Asia and other countries, and single or quadruple blinded were more likely to be published. CONCLUSIONS: GI endoscopy is rapidly evolving in clinical applications. Most clinical trials in GI endoscopy are published promptly. These findings demonstrated that investigators are active in performing and communicating the results of clinical trials in the field of GI endoscopy. In the future, the sample size calculation should be presented in detail in the registration system to maintain trial reporting transparency.

7.
J Cell Mol Med ; 24(19): 11170-11176, 2020 10.
Artigo em Inglês | MEDLINE | ID: mdl-32893994

RESUMO

Cytomegalovirus (CMV) is one of the most common intrauterine infection virus, which can cause intrauterine transmission through the placenta, resulting in abortion, stillbirth and congenital malformations. In this study, the co-culture extravillous trophoblast (EVT) HTR8/SVneo cell model of CMV infection was established in vitro. The toxicity of CMV infected EVT was determined, and then, the cell invasion experiment was conducted to evaluate the effect on the invasion ability of EVT cell lines. Western blot and real-time PCR were used to detect the related cytokines in the PI3K/AKT signalling pathway in cells. Flow cytometry was used to detect the immune function related factors of the supernatant of CMV culture on decidual NK cells. The TCID50 of CMV virus was 10-5.4 . The results of immunofluorescence showed that a large number of fluorescent green of CMV pp65 antigen signals appeared in the cytoplasm of CMV infection group. CMV could infect and replicate EVT cells and inhibited cell proliferation. The expression of proteins PDK1, AKT-S473 and AKT-S308 was significantly increased in CMV infection group. The levels of IL-17, IL-4 and IFN-γ were 8.7 ± 0.48%, 12.17 ± 0.61% and 6.66 ± 0.25%, respectively, in CMV infection group. The above results indicated that CMV infection inhibited EVT cells proliferation, weakened the invasion ability and inhibited the immune function of NK cells at the maternal-fetal interface, resulting in the abnormal maternal-fetal crosstalk.


Assuntos
Infecções por Citomegalovirus/imunologia , Células Matadoras Naturais/imunologia , Troca Materno-Fetal/imunologia , Trofoblastos/virologia , Linhagem Celular , Movimento Celular , Proliferação de Células , Citocinas/metabolismo , Infecções por Citomegalovirus/genética , Infecções por Citomegalovirus/patologia , Feminino , Humanos , Modelos Biológicos , Gravidez , Proteínas Proto-Oncogênicas c-akt/genética , Proteínas Proto-Oncogênicas c-akt/metabolismo , Piruvato Desidrogenase Quinase de Transferência de Acetil/genética , Piruvato Desidrogenase Quinase de Transferência de Acetil/metabolismo , RNA Mensageiro/genética , RNA Mensageiro/metabolismo , Trofoblastos/patologia , Proteínas da Matriz Viral/metabolismo
9.
JAAD Int ; 1(2): 77-78, 2020 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-34171033
10.
Front Med (Lausanne) ; 7: 602732, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-33537328

RESUMO

Background: Influenza was an independent risk factor for invasive pulmonary aspergillosis (IPA). In light of increasing incidence and mortality of influenza associated aspergillosis, our study summarized risk factors, clinical characteristics, and prognostic factors of developing aspergillosis in immunocompetent hosts with influenza to further screen high-risk population and improve outcome. Methods: We reviewed the patient characteristics, laboratory examinations, radiological imaging, and microbiology data of 72 influenza patients with IPA and 84 influenza patients without IPA admitted to West China Hospital. Result: Our study shown that aspergillosis co-infection increased overall mortality of severe influenza from 22.6 to 52.8%, along with higher white blood count (WBC) (10.9 ± 5.0 vs. 8.4 ± 3.3, P = 0.016), Neutrophiles (9.5 ± 5.0 vs. 7.0 ± 3.8, P = 0.023), procalcitonin (PCT) (8.6 ± 15.9 vs. 1.2 ± 2.1, P = 0.009), and a lower CD4+ T cell count (189.2 ± 135.3 vs. 367.1 ± 280.0, P = 0.022) in death group. No impact of age, gender, underlying diseases, immunosuppressive agents and steroids use, CD4+ T cell count on incidence of influenza associated aspergillosis was observed. But influenza associated aspergillosis cases mostly accompanied with more H1N1 subtype (91.7 vs. 79.8%, P = 0.037) and higher level of C-reactive protein (CRP) (117.6 ± 88.1 vs. 78.5 ± 75.2, P = 0.017) and interleukin 6 (IL-6) (133.5 ± 149.2 vs. 69.9 ± 100.0, P = 0.021) than those without aspergillosis. Conclusion: Aspergillosis co-infection in severe influenza patients can lead to a significant increased mortality, which was associated with severe respiratory failure due to mixed infection and immunosuppression. Pulmonary excessive inflammatory response was related with IPA co-infection.

11.
Front Pharmacol ; 10: 741, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31312141

RESUMO

Dysregulation of microRNAs (miRNAs) and their targeted downstream genes is involved in the carcinogenesis and progression of colorectal cancer (CRC). miR-519b-3p has been reported to play an important role in several cancers. However, its function in CRC is unclear. In this study, we detected the expression of miR-519b-3p in CRC tissues and cell lines, and determined the potential role of miR-519b-3p in cell proliferation and invasion in CRC. Also, the downstream gene of miR-519b-3p was determined. Our results showed that miR-519b-3p was notably reduced in CRC specimens and cell lines. Overexpression of miR-519b-3p inhibited the proliferation and invasion of RKO and DLD-1 cells, whereas knockdown of miR-519b-3p had the contrary effect. The ubiquitous mitochondrial creatine kinase (uMtCK) was identified as a direct target of miR-519b-3p in CRC using luciferase assay. Additionally, miR-519b-3p expression was negatively correlated with uMtCK expression in CRC specimens. Notably, the miR-519b-3p suppressed the uMtCK/Wnt signaling pathway in CRC cells, thereby suppressing CRC cell proliferation and invasion. The inhibition of uMtCK by miR-519b-3p may provide a promising option for the treatment of CRC.

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