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Surface particulates collected from the workshop floors of three major e-waste recycling sites (Taizhou, Qingyuan, and Guiyu) in China were analyzed for tetrabromobisphenol A/S (TBBPA/S) and their derivatives to investigate the environmental pollution caused by e-waste recycling activities. Mean concentrations of total TBBPA/S analogs in surface particulates were 31,471-116,059 ng/g dry weight (dw). TBBPA, TBBPA-BGE, and TBBPA-BDBPE were the most frequently detected in particulates with average concentration ranges of 17,929-78,406, 5601-15,842, and 5929-21,383 ng/g dw, respectively. Meanwhile, TBBPA, TBBPA-BGE, and TBBPA-BDBPE were the most abundant TBBPA/S analogs, accounting for around 96% of the total. The composition profiles of TBBPA/S analogs differed significantly among three e-waste sites. Similarly, principal component analysis uncovered different pollution patterns among different sites. The discrepancy in the profiles of TBBPA/S analogs largely relied on the e-waste types recycled in different areas. E-waste recycling led to the release of TBBPA/S analogs, and TBBPA/S analogs produced differentiation during migration from source (surface particulates) to nearby soil. More researches are necessary to find a definite relationship between pollution status and e-waste types and study differentiation behavior of TBBPA/S analogs in migration and diffusion from source to environmental medium.
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Resíduo Eletrônico , Monitoramento Ambiental , Bifenil Polibromatos , Reciclagem , Bifenil Polibromatos/análise , China , Resíduo Eletrônico/análise , Material Particulado/análiseRESUMO
Glycolytic reprogramming is one of the most important features of cancer and plays an integral role in the progression of cancer. In cancer cells, changes in glucose metabolism meet the needs of self-proliferation, angiogenesis and lymphangiogenesis, metastasis, and also affect the immune escape, prognosis evaluation and therapeutic effect of cancer. The n6-methyladenosine (m6A) modification of RNA is widespread in eukaryotic cells. Dynamic and reversible m6A modifications are widely involved in the regulation of cancer stem cell renewal and differentiation, tumor therapy resistance, tumor microenvironment, tumor immune escape, and tumor metabolism. Lately, more and more evidences show that m6A modification can affect the glycolysis process of tumors in a variety of ways to regulate the biological behavior of tumors. In this review, we discussed the role of glycolysis in tumor genesis and development, and elaborated in detail the profound impact of m6A modification on different tumor by regulating glycolysis. We believe that m6A modified glycolysis has great significance and potential for tumor treatment.
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Neoplasias , Humanos , Neoplasias/genética , Epigênese Genética , Glicólise , Epigenômica , Adenosina , Microambiente Tumoral/genéticaRESUMO
OBJECTIVE: To compare the short- and long-term outcomes of robot-assisted (RALR), laparoscopic (LLR), or open liver resection (OLR) in the treatment of Barcelona Clinic Liver Cancer (BCLC) stage 0-A hepatocellular carcinoma (HCC). SUMMARY BACKGROUND DATA: Following the Balliol IDEAL classification, long-term oncological outcomes can be used to evaluate the value of minimally invasive techniques in the treatment of HCC, and to assess whether they should become a standard practice. METHODS: Data from prospective cohorts of patients with BCLC stage 0-A HCC who underwent curative liver resection using OLR, LLR, or RALR at Tongji Hospital were reviewed. The short-term and long-term oncological outcomes of these 3 different surgical approaches after adequate follow-up were compared using propensity score matching to reduce selection bias. RESULTS: Of 369 patients included in this study (71, RALR; 141, LLR; and 157, OLR), 56 patients in each of the 3 groups were chosen for further comparison, after propensity score matching. In the minimally invasive group (RALR+LLR), both the operative time and duration of Pringle's maneuver were significantly longer than those in the OLR group; however, the length of hospital stay was significantly shorter. There were no significant differences in the other intraoperative parameters and the incidence of postoperative complications among the 3 groups. HCC recurrence in the minimally invasive group when compared with the OLR group was characterized by a significantly higher proportion of single lesion or early-stage HCC. However, there were no significant differences in the 5-year disease-free survival (63.8%, 54.4%, and 50.6%) or overall survival rates (80.8%, 78.6%, and 75.7%, respectively) among the 3 groups. Clinically significant portal hypertension was the only risk factor that negatively affected the 5-year disease-free survival rate. Multivariate Cox regression analysis showed that clinically significant portal hypertension, serum alpha-fetoprotein level (≥400 ng/mL), and Edmondson-Steiner grading (III+IV) were independent risk factors for poor long-term survival. CONCLUSION: Both robotic and laparoscopic hepatectomies were safe and effective for patients with BCLC stage 0-A HCC when compared with open hepatectomy.
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Carcinoma Hepatocelular , Hipertensão Portal , Laparoscopia , Neoplasias Hepáticas , Procedimentos Cirúrgicos Robóticos , Humanos , Carcinoma Hepatocelular/cirurgia , Hepatectomia/métodos , Hipertensão Portal/etiologia , Laparoscopia/métodos , Tempo de Internação , Neoplasias Hepáticas/cirurgia , Complicações Pós-Operatórias/epidemiologia , Pontuação de Propensão , Estudos Prospectivos , Estudos RetrospectivosRESUMO
Cancer stem cells (CSCs) have been blamed as the main culprit of tumor initiation, progression, metastasis, chemoresistance, and recurrence. However, few anti-CSCs agents have achieved clinical success so far. Here we report a novel derivative of lonidamine (LND), namely HYL001, which selectively and potently inhibits CSCs by targeting mitochondria, with 380-fold and 340-fold lower IC50 values against breast cancer stem cells (BCSCs) and hepatocellular carcinoma stem cells (HCSCs), respectively, compared to LND. Mechanistically, we reveal that HYL001 downregulates glutaminase (GLS) expression to block glutamine metabolism, blunt tricarboxylic acid cycle, and amplify mitochondrial oxidative stress, leading to apoptotic cell death. Therefore, HYL001 displays significant antitumor activity in vivo, both as a single agent and combined with paclitaxel. Furthermore, HYL001 represses CSCs of fresh tumor tissues derived from liver cancer patients. This study provides critical implications for CSCs biology and development of potent anti-CSCs drugs.
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Antineoplásicos , Neoplasias Hepáticas , Humanos , Antineoplásicos/farmacologia , Antineoplásicos/uso terapêutico , Antineoplásicos/metabolismo , Glutamina/metabolismo , Neoplasias Hepáticas/tratamento farmacológico , Neoplasias Hepáticas/metabolismo , Mitocôndrias/metabolismo , Células-Tronco Neoplásicas , Linhagem Celular TumoralRESUMO
The low-oxidation-state silicon-catalyzed hydroboration of isocyanates with pinacolborane (HBpin) using the NHC-silyliumylidene cation catalyst [(IMe)2SiH]I (1, IMe = :C{N(Me)C(Me)}2) is described. In the catalysis, the Si lone pair electrons activate isocyanates, and the latter react with HBpin to form N-boryl formamides at room temperature. Catalyst 1 further activates N-boryl formamides at 70 °C, the intermediates of which react with HBpin to form N-boryl methylamines and (pinB)2O.
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BACKGROUND: Ingestion of fish bones leading to gastric perforation and inducing abscess formation in the caudate lobe of the liver is very rare. CASE PRESENTATION: A 67-year-old man presented to our hospital with a 2-day history of subxiphoid pain. There were no specific symptoms other than pain. Laboratory tests showed only an increase in the number and percentage of neutrophils. Contrast-enhanced Computerized tomography (CT) of the abdomen showed two linear dense opacities in the gastric cardia, one of which penetrated the stomach and was adjacent to the caudate lobe of the liver, with inflammatory changes in the caudate lobe. We finally diagnosed his condition as a caudate lobe abscess secondary to intestinal perforation caused by a fishbone based on the history and imaging findings. The patient underwent 3D laparoscopic partial caudate lobectomy, incision and drainage of the liver abscess, and fishbone removal. The procedure was successful and we removed the fishbone from the liver. The patient was discharged on the 9th postoperative day without other complications. CONCLUSIONS: Liver abscess caused by foreign bodies requires multidisciplinary treatment. Especially when located in the caudate lobe, we must detect and remove the cause of the abscess as early as possible. Foreign bodies that perforate the gastrointestinal tract can penetrate to the liver and cause abscess formation, as in this case. When exploring the etiology of liver abscesses, we should investigate the general condition, including the whole gastrointestinal tract.
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Corpos Estranhos , Migração de Corpo Estranho , Laparoscopia , Abscesso Hepático , Idoso , Animais , Corpos Estranhos/complicações , Corpos Estranhos/diagnóstico por imagem , Corpos Estranhos/cirurgia , Migração de Corpo Estranho/complicações , Migração de Corpo Estranho/diagnóstico por imagem , Migração de Corpo Estranho/cirurgia , Humanos , Abscesso Hepático/diagnóstico por imagem , Abscesso Hepático/etiologia , Abscesso Hepático/cirurgia , MasculinoRESUMO
While the concept of environmental sustainability has steadily grown over the past thirty years, little progress has been made in unifying the efforts of the entities most involved: society, the environment, the economy, and governmental policy. This synthesis integrates across disciplines to outline the need for a harmonized sustainability model to align disparate environmental objectives. Specifically, this study highlights the disconnect between policy and capitalistic economies regarding environmental sustainability. We then provide a framework for an updated sustainability model and offer pathways toward an improved state of environmental sustainability. Notable contributions include the development of a dynamic, harmonized sustainability model derived from basic supply and demand curves that functions for both the consumption and disposal of resources at multiple scales.
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Conservação dos Recursos Naturais , PolíticasRESUMO
The TGF-ß receptor kinase inhibitors (TRKI) have been reported to inhibit tumorigenicity in colon cancer. However, there is no direct evidence showing that these inhibitors function through inhibiting the TGF-ß- mediated tumor-promoting effects in vivo. We established a TGF-ß inducible reporter system by inserting a luciferase reporter gene to the vector downstream of TGF-ß-inducible promoter elements, and transfected it into colon cancer cell lines. TRKIs SB431542 and LY2109761 were used to treat TGF-ß inducible cells in vitro and in vivo. The luciferase activity was induced 5.24-fold by TGF-ß in CT26 inducible cells, while it was marginally changed in MC38 inducible cells lacking Smad4 expression. Temporary treatment of mice with SB431542 inhibited the TGF-ß pathway and TGF-ß induced bioluminescence activity in vivo. Long-term treatment with LY2109761 inhibited tumorigenicity and liver metastasis in vivo in concomitant with reduced luciferase activity in the tumor. In this study, we established a model to monitor the TGF-ß pathway in vivo and to compare the antitumor effects of TRKIs. Based on this novel experimental tool, we provided direct evidences that LY2109761 inhibits tumorigenicity and liver metastasis by blocking the pro-oncogenic functions of TGF-ß in vivo.
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Carcinogênese/efeitos dos fármacos , Neoplasias do Colo/tratamento farmacológico , Receptores de Fatores de Crescimento Transformadores beta/genética , Fator de Crescimento Transformador beta/genética , Animais , Benzamidas/farmacologia , Linhagem Celular Tumoral , Proliferação de Células/efeitos dos fármacos , Neoplasias do Colo/genética , Neoplasias do Colo/patologia , Dioxóis/farmacologia , Modelos Animais de Doenças , Humanos , Camundongos , Inibidores de Proteínas Quinases/farmacologia , Pirazóis/farmacologia , Pirróis/farmacologia , Receptores de Fatores de Crescimento Transformadores beta/antagonistas & inibidores , Transdução de Sinais/efeitos dos fármacosRESUMO
Skin wound is a very common type of injury and the healing process greatly affects the life quality of individuals. Ozone has been shown beneficial to wound healing with unclear mechanisms. Here, we tested the effect of ozone oil (OZ) on wound healing and investigated the underlying mechanisms. Mouse skin wound model and Masson staining were used to evaluate the effect of OZ on wound healing. Primary fibroblast culture was employed to assess the functions of OZ, miR-21-5p, and RASA1. QRT-PCR and western blot were used to determine expression levels of miR-21-5p, RASA1, α-SMA, and collagen I. CCK-8 assay and scratch wound healing assay were used to measure viability and migration of fibroblasts. Dual luciferase activity assay was performed to validate miR-21-5p/RASA1 interaction. OZ accelerated wound healing in mice and promoted proliferation and migration abilities of fibroblasts. miR-21-5p was increased while RASA1 was reduced during the wound healing and OZ treatment augmented those changes, as well as increased levels of α-SMA and collagen I. Knockdown of miR-21-5p suppressed those effects of OZ on fibroblasts. Furthermore, miR-21-5p directly targeted RASA1 mRNA and negatively regulated its expression. Overexpression of RASA1 inhibited fibroblast proliferation and migration as well as diminished α-SMA and collagen I protein expression. Additionally, RASA1 overexpression blocked the promotion of miR-21-5p overexpression on fibroblast viability and migration. In vivo, miR-21-5p facilitated wound healing while overexpression of RASA1 reversed the effect. OZ promoted wound healing by enhancing miR-21-5p-mediated RASA1 inhibition to increase fibroblast proliferation and migration.
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MicroRNAs , Ozônio , Animais , Movimento Celular , Fibroblastos , Camundongos , MicroRNAs/genética , Ozônio/farmacologia , CicatrizaçãoRESUMO
Compared with the standard depolarization index, indices of polarimetric purity (IPPs) have better performances to describe depolarization characteristics of targets with different roughnesses of interfaces under different incident angles, which allow us a further analysis of the depolarizing properties of samples. Here, we use IPPs obtained from different reflective interfaces as a criterion of depolarization property to characterize and classify targets covered by organic paint layers with different roughness. We select point-light source as radiation source with wavelength as 632.8 nm, and four samples, including Cu, Au, Al and Al2O3, covered by an organic paint layer with refractive index of n = 1.46 and Gaussian roughness of α = 0.05~0.25. Under different incident angles, the values of P1, P2, P3 at divided 90 × 360 grid points and their mean values in upper hemisphere have been obtained and discussed in the IPPs space. The results show that the depolarization performances of the different reflective interfaces (materials, incident angles and surface roughness) are unique in IPPs space, providing us with a new avenue to analyze and characterize different targets.
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The Internet of Vehicle (IoV) technology is one of the most important technologies of modern intelligent transportation. The data transmission scheduling method is a research hotspot in the technology of IoV. It is a challenge to ensure the stability of data transmission due to fast network topology changes, high data transmission delays, and some other reasons. Aiming at the above problems, a multi-channel data transmission cooperative scheduling algorithm is proposed. First, construct a feasible interference map based on the data items sent and received by vehicles in the road scene. Second, assign channels to the nodes in the interference map based on the Signal-to-Interference-Noise-Ratio (SINR). Finally, the optimal multi-channel data transmission cooperative scheduling scheme is achieved through the ISing model. Simulation results show that compared with the traditional algorithm, the network service capacity is increased by about 31% and the service delay is reduced by about 20%. It ensures that emergency data is preferentially transmitted to the target vehicle and the maximum weighted service capacity of the network.
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DNA methylation is a crucial regulator of gene transcription in the etiology and pathogenesis of hepatocellular carcinoma (HCC). Thus, it is reasonable to identify DNA methylation-related prognostic markers. Currently, we aimed to make an integrative epigenetic analysis of HCC to identify the effectiveness of epigenetic drivers in predicting prognosis for HCC patients. By the software pipeline TCGA-Assembler 2, RNA-seq, and methylation data were downloaded and processed from The Cancer Genome Atlas. A bioconductor package MethylMix was utilized to incorporate gene expression and methylation data on all 363 samples and identify 589 epigenetic drivers with transcriptionally predictive. By univariate survival analysis, 72 epigenetic drivers correlated with overall survival (OS) were selected for further analysis in our training cohort. By the robust likelihood-based survival model, six epi-drivers (doublecortin domain containing 2, flavin containing monooxygenase 3, G protein-coupled receptor 171, Lck interacting transmembrane adaptor 1, S100 calcium binding protein P, small nucleolar RNA host gene 6) serving as prognostic markers was identified and then a DNA methylation signature for HCC (MSH) predicting OS was identified to stratify patients into low-risk and high-risk groups in the training cohort (p < 0.001). The capability of MSH was also assessed in the validation cohort (p = 0.002). Furthermore, a receiver operating characteristic curve confirmed MSH as an effective prognostic model for predicting OS in HCC patients in training area under curve (AUC = 0.802) and validation (AUC = 0.691) cohorts. Finally, a nomogram comprising MSH and pathologic stage was generated to predict OS in the training cohort, and it also operated effectively in the validation cohort (concordance index: 0.674). In conclusion, MSH, a six epi-drivers based signature, is a potential model to predict prognosis for HCC patients.
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Carcinoma Hepatocelular/genética , Metilação de DNA/fisiologia , Regulação Neoplásica da Expressão Gênica/genética , Neoplasias Hepáticas/genética , Biomarcadores Tumorais/genética , Carcinoma Hepatocelular/metabolismo , Epigenômica/métodos , Feminino , Perfilação da Expressão Gênica/métodos , Humanos , Neoplasias Hepáticas/diagnóstico , Neoplasias Hepáticas/patologia , Masculino , Pessoa de Meia-Idade , Prognóstico , Curva ROCRESUMO
This study describes the first use of a silicon(II) complex, NHC-parent silyliumylidene cation complex [(IMe)2SiH]I (1, IMe = :C{N(Me)C(Me)}2) as a versatile catalyst in organic synthesis. Complex 1 (loading: 10 mol %) was shown to act as an efficient catalyst (reaction time: 0.08 h, yield: 94%, TOF = 113.2 h-1; reaction time: 0.17 h, yield: 98%, TOF = 58.7 h-1) for the selective reduction of CO2 with pinacolborane (HBpin) to form the primarily reduced formoxyborane [pinBOC(âO)H]. The activity is better than the currently available base-metal catalysts used for this reaction. It also catalyzed the chemo- and regioselective hydroboration of carbonyl compounds and pyridine derivatives to form borate esters and N-boryl-1,4-dihydropyridine derivatives with quantitative conversions, respectively. Mechanistic studies show that the silicon(II) center in complex 1 activated the substrates and then mediated the catalytic hydroboration. In addition, complex 1 was slightly converted into the NHC-borylsilyliumylidene complex [(IMe)2SiBpin]I (3) in the catalysis, which was also able to mediate the catalytic hydroboration.
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OBJECTIVE: To study the expression levels of glial cell line-derived neurotrophic factor family receptor α-1 (GFRα1) and enhancer of zeste homolog 2 (EZH2) in the intestinal tissue of children with Hirschsprung's disease (HSCR), as well as the role of EZH2 in the regulation of GFRα1 gene expression and the pathogenesis of HSCR. METHODS: The samples of colon tissue with spasm from 24 children with HSCR after radical treatment of HSCR were selected as the experimental group, and the samples of necrotized colon tissue from 18 children with neonatal necrotizing enterocolitis after surgical resection were selected as the control group. Real-time PCR and Western blot were used to measure the expression levels of GFRα1 and EZH2 in colon tissue in both groups. Human neuroblastoma SH-SY5Y cells were divided into an EZH2 over-expression group and a negative control group. The cells in the EZH2 over-expression group were transfected with pCMV6-EZH2 plasmid, and those in the negative control group were transfected with pCMV6 plasmid. The expression levels of EZH2 and GFRα1 were measured after transfection. RESULTS: Compared with the control group, the experimental group had significant reductions in the mRNA and protein expression levels of GFRα1 and EZH2 in colon tissue (P<0.05), and the protein expression of EZH2 was positively correlated with that of GFRα1 (r=0.606, P=0.002). Compared with the negative control group, the EZH2 over-expression group had significant increases in the expression levels of EZH2 and GFRα1 after SH-SY5Y cells were transfected with EZH2 over-expression plasmid (P<0.05). CONCLUSIONS: Low expression of EZH2 in the colon tissue of children with HSCR may be one of the causes of inadequate expression of GFRα1 and onset of HSCR.
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Proteína Potenciadora do Homólogo 2 de Zeste/genética , Receptores de Fator Neurotrófico Derivado de Linhagem de Célula Glial/genética , Doença de Hirschsprung , Criança , Colo , Doença de Hirschsprung/genética , Humanos , Recém-Nascido , RNA MensageiroRESUMO
BACKGROUND/AIMS: Cholestasis is characterized by intrahepatic accumulation of cytotoxic bile acids (BAs), ultimately leading to fibrosis and cirrhosis, but the precise role of BAs in cholestasis-induced liver fibrosis remains largely elusive. In this study, we investigated the role and the potential mechanisms of BAs during cholestasis in vivo and in vitro. METHODS: The effect of BAs during cholestasis was studied in bile duct ligation (BDL) rat models in vivo. We performed immunohistochemistry, Western blotting, and quantitative RT-PCR to investigate the expression of connective tissue growth factor (CTGF/CCN2) in rat liver during cholestasis. The hepatic cell lines AML12 and BRL were stimulated with taurocholate (TC) and the level of CTGF/CCN2, and activation of ERK, Akt, p38 MAPK, JNK, YAP, and TGF-ß/Smad signaling were examined using Western blotting. Next, to elucidate the mechanism underlying bile acid-induced CTGF/CCN2, we treated the cells with MEK1/2 inhibitor (U0126), YAP function inhibitor (verteporfin), p38 kinase inhibitor (SB203580), Akt inhibitor (MK2206), and small interfering RNA (siRNA) targeting mek1, erk, and yap in cooperation with TC. Besides, we confirmed the activation of these signaling pathways in BDL and sham rat livers by immunohistochemistry, Western blotting, and quantitative RT-PCR. RESULTS: In this study, we confirmed that the expression of CTGF/CCN2 was increased in BDL-induced rodent cholestatic liver fibrosis. In addition, we showed that TC, the main component of BAs, enhanced the synthesis of CTGF/ CCN2 in AML12 and BRL hepatic cell lines. Moreover, we demonstrated that TC activated ERK, Akt, and YAP signaling in hepatocytes, but the precise roles of these signaling cascades in the expression of CTGF/CCN2 were different: TC-induced expression of CTGF/CCN2 was mediated by ERK-YAP signaling, whereas Akt signaling inhibited ERK signaling and YAP and subsequently the expression of CTGF/CCN2 in hepatocytes. Furthermore, YAP functioned as a downstream regulator of ERK signaling in TC-induced CTGF/CCN2 expression in hepatocytes. CONCLUSION: Our report provides evidence for the role of conjugated BAs in liver fibrosis and suggests that the production of CTGF/CCN2, induced by conjugated BAs via ERK-YAP axis activation, may be a therapeutic target in cholestasis-induced liver fibrosis.
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Proteínas Reguladoras de Apoptose/metabolismo , Fator de Crescimento do Tecido Conjuntivo/metabolismo , MAP Quinases Reguladas por Sinal Extracelular/metabolismo , Transdução de Sinais/efeitos dos fármacos , Ácido Taurocólico/farmacologia , Animais , Proteínas Reguladoras de Apoptose/antagonistas & inibidores , Proteínas Reguladoras de Apoptose/genética , Butadienos/farmacologia , Linhagem Celular , Colestase/etiologia , Colestase/metabolismo , MAP Quinases Reguladas por Sinal Extracelular/antagonistas & inibidores , MAP Quinases Reguladas por Sinal Extracelular/genética , Hepatócitos/citologia , Hepatócitos/efeitos dos fármacos , Hepatócitos/metabolismo , Fígado/metabolismo , Fígado/patologia , MAP Quinase Quinase 1/antagonistas & inibidores , MAP Quinase Quinase 1/genética , MAP Quinase Quinase 1/metabolismo , Masculino , Nitrilas/farmacologia , Porfirinas/farmacologia , Proteínas Proto-Oncogênicas c-akt/antagonistas & inibidores , Proteínas Proto-Oncogênicas c-akt/metabolismo , Interferência de RNA , RNA Interferente Pequeno/metabolismo , Ratos , Ratos Sprague-Dawley , Regulação para Cima/efeitos dos fármacos , Verteporfina , Proteínas de Sinalização YAPRESUMO
BACKGROUND: This study explored the effect of liver resection on perioperative circulating tumor cells (CTCs) and found that the prognostic significance of surgery was associated with changes in CTC counts in patients with hepatocellular carcinoma (HCC). METHODS: One hundred thirty-nine patients with HCC were consecutively enrolled. The time-points for collecting blood were one day before operation and three days after operation. CTCs in the peripheral blood were detected by the CellSearch™ System. RESULTS: Both CTC detection incidence and mean CTC counts showed greater increases postoperatively (54%, mean 1.54 cells) than preoperatively (43%, mean 1.13 cells). The postoperative CTC counts increased in 41.7% of patients, decreased in 25.2% of patients and did not change in 33.1% of patients. The increase in postoperative CTC counts was significantly associated with the macroscopic tumor thrombus status. Patients with increased postoperative CTC counts (from preoperative CTC < 2 to postoperative CTC ≥ 2) had significantly shorter disease-free survival (DFS) and overall survival (OS) than did patients with persistent CTC < 2. Patients with persistent CTC levels of ≥2 had the worst prognoses. CONCLUSIONS: Surgical liver resection is associated with an increase in CTC counts, and increased postoperative CTC numbers are associated with a worse prognosis in patients with HCC.
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Biomarcadores Tumorais/sangue , Carcinoma Hepatocelular/cirurgia , Hepatectomia/efeitos adversos , Neoplasias Hepáticas/cirurgia , Células Neoplásicas Circulantes , Adulto , Idoso , Idoso de 80 Anos ou mais , Contagem de Células Sanguíneas/métodos , Carcinoma Hepatocelular/sangue , Carcinoma Hepatocelular/patologia , Intervalo Livre de Doença , Feminino , Humanos , Fígado/patologia , Fígado/cirurgia , Neoplasias Hepáticas/sangue , Neoplasias Hepáticas/patologia , Masculino , Pessoa de Meia-IdadeRESUMO
BACKGROUND: Isocitrate dehydrogenase 1/2 (IDH1/2) mutations have been reported in intrahepatic cholangiocarcinoma (IHCC). However, the prognosis of a single IDH1 mutation and impact of mutant IDH1 on IHCC tumor growth remain unclear. METHODS: A total of 85 IHCC tumor samples were sequenced. Prognosis and clinicopathological correlation were analyzed. The role of mutant IDH1 in IHCC tumor growth was measured by cell proliferation assay, colony formation assay in soft agar, and xenograft tumor models. Akt, ERK, p38 MAPK, and JNK signaling, which commonly affect tumor growth, were examined by Western blotting to explore the potential mechanism. RESULTS: IDH1 mutations correlated with a beneficial prognosis and smaller tumor size. Mutant IDH1 exhibited a growth-inhibitory effect on IHCC cell lines in vitro and in vivo. Akt signaling was suppressed in IHCC cell lines expressing a mutant IDH1. The reactivation of Akt signaling by SC79 restored the inhibited growth of cell lines expressing a mutant IDH1 in IHCC. CONCLUSIONS: Collectively, we demonstrated that mutant IDH1 correlates with a beneficial prognosis and inhibits tumor growth by suppressing Akt signaling in IHCC. We suggest that patients with IDH1 mutations could be considered for both less-aggressive therapy and therapy tailored to the presence of their mutant enzyme in the future.
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Neoplasias dos Ductos Biliares/genética , Colangiocarcinoma/genética , Isocitrato Desidrogenase/genética , Neoplasias dos Ductos Biliares/metabolismo , Linhagem Celular Tumoral , Proliferação de Células , Colangiocarcinoma/metabolismo , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Mutação , Proteínas Proto-Oncogênicas c-akt/metabolismoRESUMO
BACKGROUND: To evaluate the safety and efficacy of IOUS in robotic liver surgery and propose a standard protocol of IOUS for safe robot-assisted hepatectomy. METHODS: Between February 2015 and December 2016, liver resection was performed in 110 patients with robotic approach in Tongji Hospital. In these patients, IOUS was routinely performed. All data about demographic, surgical procedure, postoperative course were collected prospectively and analyzed. RESULTS: A four steps IOUS protocol in robotic liver surgery was proposed, including exploration, verification, guidance, and confirmation. A total of 11 additional lesions in 11 patients were detected and 7 patients accepted strategic surgical modification. No patient suffered from any single or multiple organ dysfunctions, and there were no mortalities observed. CONCLUSION: IOUS is indispensable to understand lesions and vessels in robotic liver surgery. A four-step standard protocol of IOUS is essential for safe robot-assisted hepatectomy.
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Hepatectomia/métodos , Laparoscopia/métodos , Neoplasias Hepáticas/cirurgia , Procedimentos Cirúrgicos Robóticos/métodos , Cirurgia Assistida por Computador/métodos , Ultrassonografia/métodos , Feminino , Humanos , Período Intraoperatório , Neoplasias Hepáticas/diagnóstico , Masculino , Pessoa de Meia-Idade , Reprodutibilidade dos TestesRESUMO
The general clinical procedure for viral DNA detection or gene mutation diagnosis following polymerase chain reaction (PCR) often involves gel electrophoresis and DNA sequencing, which is usually time-consuming. In this study, we have proposed a facile strategy to construct a DNA biosensor, in which the platinum electrode was modified with a dual-film of electrochemically synthesized poly(3,4-ethylenedioxythiophene) (PEDOT) resulting in immobilized gold nanoparticles, with the gold nanoparticles easily immobilized in a uniform distribution. The DNA probe labeled with a SH group was then assembled to the fabricated electrode and employed to capture the target DNA based on the complementary sequence. The hybridization efficiency was evaluated with differential pulse voltammetry (DPV) in the presence of daunorubicin hydrochloride. Our results demonstrated that the peak current in DPV exhibited a linear correlation the concentration of target DNA that was complementary to the probe DNA. Moreover, the electrode could be reused by heating denaturation and re-hybridization, which only brought slight signal decay. In addition, the addition of the oxidized form of nicotinamide adenine dinucleotide (NADâº) could dramatically enhance the sensitivity by more than 5.45-fold, and the limit-of-detection reached about 100 pM.
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Técnicas Biossensoriais/métodos , Compostos Bicíclicos Heterocíclicos com Pontes/química , DNA/análise , Condutividade Elétrica , Polímeros/química , Temperatura , Técnicas Eletroquímicas , Eletrodos , Ouro , Nanopartículas Metálicas , Platina/química , Poliestirenos/químicaRESUMO
In wireless network communication, in-band full-duplex technique is a useful and important technique that can enlarge the whole throughput of the wireless networks. However, its use needs harsh environment. The successive interference cancellation can make several transmitters' data be received simultaneously by the receiver, and can make the in-band full-duplex technique be used easily in reality. In this paper, we try to propose an optimal algorithm for increasing the throughput of full-duplex multi-hop wireless networks with successive interference cancellation, which we call the full-duplex successive interference cancellation (FD-SIC) wireless networks. We first describe the mathematical model for the FD-SIC wireless networks and show it is NP-hard in general. Then, we propose a heuristic algorithm, namely the use-up-link-capacity iterative (UULC-iterative) algorithm, for each node's routing and transmitting scheme. Simulation results show that the proposed algorithm for FD-SIC wireless networks can achieve better throughput compared with SIC-only networks and the interference avoidance networks.