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1.
Medicine (Baltimore) ; 100(34): e26681, 2021 Aug 27.
Artigo em Inglês | MEDLINE | ID: mdl-34449453

RESUMO

RATIONALE: Recently, the number of osteosarcomas has been increasing in elderly patients due to human longevity. Lung metastases are the primary cause of death from osteosarcomas. Complete resection of lung metastases can prolong the survival. However, complete resection in elderly patients is often difficult due to high risk of operative complications. Computed tomography (CT) guided radiofrequency ablation (RFA) is a minimally invasive technique to destroy tumor nodules using heat. In this report, we present the first case older than 65 years applying RFA for lung metastases due to osteosarcoma. PATIENT CONCERNS: A 74-year-old male presented with 1-year history of heel pain. A conventional high-grade osteosarcoma in his calcaneus was diagnosed. Below-knee amputation was performed. However, lung metastases were found in both lungs 1 year after amputation. CT-guided lung RFA was chosen since surgical intervention for lung metastases was abandoned because of tumor multiplicity and medical comorbidities. A total of 18 lung metastases were treated by CT-guided RFA. The most frequent complication was pneumothoraxes in 4 of 8 (50%) procedures and chest tube drainage was required in 2 of these (2 of 8 (25%) procedures). DIAGNOSES: Six lung metastases of osteosaroma were found in both lungs at 1 year after surgery. INTERVENTIONS: CT-guided lung RFA was performed. A total of 18 lung metastases were treated in 8 lung RF procedures. OUTCOMES: The patient has been alive with disease for 5.5 years after the initial surgery. LESSONS: CT-guided lung RFA is effective for elderly patients with osteosarcoma lung metastases in spite of discouragement of lung metastasectomy due to multiplicity of metastases and medical-comorbidities.


Assuntos
Neoplasias Ósseas/patologia , Neoplasias Pulmonares/secundário , Neoplasias Pulmonares/cirurgia , Osteossarcoma/patologia , Ablação por Radiofrequência/métodos , Idoso , Calcâneo/patologia , Humanos , Masculino , Radiografia Intervencionista , Tomografia Computadorizada por Raios X
2.
Hepatol Res ; 49(6): 676-686, 2019 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-30680865

RESUMO

AIM: Transient elastography (TE) is the gold standard for measurement of liver stiffness. The usefulness of shear wave elastographies (SWE) is well accepted. However, the measurement values cannot be equivalently compared because cut-off values for the diagnosis of liver fibrosis are different among those devices. We aimed to clarify correlations, to generate the regression equations between TE and SWEs, and to compare the diagnostic ability of each device to diagnose liver fibrosis. METHODS: A total of 109 patients with chronic liver disease who underwent liver biopsy and same-day evaluation of liver stiffness using six ultrasound devices were analyzed. The diagnostic ability of liver stiffness from each ultrasound device and correlations between TE and each SWE were analyzed. RESULTS: Liver stiffness measured by all six ultrasound devices increased significantly as liver fibrosis stage advanced (P < 0.001). Receiver operating characteristic (ROC) curve analysis for predicting significant fibrosis (≥F2) and cirrhosis yielded area under the ROC curve (AUROC) values based on TE of 0.830 (95% confidence interval [CI], 0.755-0.905) and 0.959 (95% CI, 0.924-0.995), respectively. The AUROCs for predicting significant fibrosis (≥F2) and cirrhosis (F4) based on SWE from all five ultrasound devices were over 0.8 and 0.9, respectively. Furthermore, the correlation coefficients between TE values and SWE values from five ultrasound devices were all over 0.8, indicating a strong relationship. CONCLUSION: Our study showed strong correlations between TE and SWEs with high correlation coefficients. The regression equations between TE and SWEs demonstrated the ability to compare the measurement values in each device equivalently.

3.
J Surg Case Rep ; 2017(7): rjx139, 2017 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-28775837

RESUMO

A Japanese baby was born with a polypoidal projection with hair, on the lateral corner of upper eyelid. The tumour had extent to bulbar sub-conjunctival area. He presented no other malformation nor pathological symptoms. There was no sign of association with Goldenhar, hemifacial macrosomia, epidermal nevus or linear nevus sebaceous syndromes. The tumour was resected at his age of 4 months. The ocular conjunctiva was incised but not excised. Histopathologically, it was mainly consisted of multi-lobuled mature adipose tissue, dense fibrous tissue was observed at the centre of mass, assumed to be the link of palpebral tarsal plate to lateral canthal ligament. As for the location and component, the tumour was diagnosed as a lipomatous hamartoma. Detached tarsal plate was reattached to the lateral canthal ligament. Satisfactory result was achieved aesthetically and functionally. Congenital lipomatous hamartoma, with protuberant appendage appearance on eyelid, without syndromic association, is presented.

6.
Pathol Res Pract ; 211(5): 415-20, 2015 May.
Artigo em Inglês | MEDLINE | ID: mdl-25749627

RESUMO

We experienced a rare case of penile mesenchymal tumor in a 43-year-old Japanese man. At least three nodules were observed around the penis. The tumors were composed of spindle- to oval-shaped atypical cells with and without prominent nucleoli. These cells were like myogenic cells, but negative for myogenic markers. They were positive for endothelial markers, such as ERG, Fli1 and CD31. They were also positive for nuclear and cytoplasmic FOSB which are not expressed in epithelioid hemangioendothelioma or epithelioid sarcoma. These pathological and immunohistochemical findings strongly suggested pseudomyogenic hemangioendothelioma/epithelioid sarcoma-like hemangioendothelioma (PHE/ES-HE). Since a recent report directly proved that two cases of PHE/ES-HE have SERPINE1-FOSB fusion gene by reverse transcription-polymerase chain reaction (RT-PCR), we examined whether the fusion gene is present or not in the present case by RT-PCR using fresh frozen surgical material. Sequencing of the PCR product revealed that this case has SERPINE1-FOSB fusion. The fusion pattern of our case was different from those of two previously reported cases. In our case, 86 nucleotides of SERPINE1 intron 1 were inserted between SERPINE1 exon 1 and the middle portion of FOSB exon 1, and a putative translation start codon was identified in SERPINE1 intron 1. Thus, this is the third case of PHE/ES-HE with SERPINE1-FOSB fusion proved by RT-PCR.


Assuntos
Hemangioendotelioma/genética , Proteínas de Fusão Oncogênica/genética , Neoplasias Penianas/genética , Inibidor 1 de Ativador de Plasminogênio/genética , Proteínas Proto-Oncogênicas c-fos/genética , Adulto , Biomarcadores Tumorais/análise , Hemangioendotelioma/patologia , Humanos , Imuno-Histoquímica , Masculino , Neoplasias Penianas/patologia , Reação em Cadeia da Polimerase Via Transcriptase Reversa
7.
J Gastroenterol ; 47(10): 1143-51, 2012 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-22441534

RESUMO

BACKGROUND: This study explores pretreatment predictive factors for ultimate virological responses to pegylated interferon-α (1.5 µg/kg/week) and ribavirin (600-1000 mg/day) (PEG-IFN/RBV) combination therapy for patients infected with hepatitis C virus (HCV)-1b and a high viral load. METHODS: A total of 75 patients underwent PEG-IFN/RBV combination therapy for 48 weeks. HCV amino acid (aa) substitutions in non-structural protein 5a, including those in the IFN/RBV resistance-determining region (IRRDR) and the IFN sensitivity-determining region and the core regions, as well as the genetic variation (rs8099917) near the interleukin 28B (IL28B) gene (genotype TT) were analyzed. RESULTS: Of the 75 patients, 49 % (37/75) achieved a sustained virological response (SVR), 27 % (20/75) showed relapse, and 24 % (18/75) showed null virological response (NVR). Multivariate logistic regression analysis identified IRRDR with 6 or more mutations (IRRDR ≥6) [odds ratio (OR) 11.906, p < 0.0001] and age <60 years (OR 0.228, p = 0.015) as significant determiners of SVR and IL28B minor (OR 14.618, p = 0.0019) and platelets <15 × 10(4)/mm(3) (OR 0.113, p = 0.0096) as significant determiners of NVR. A combination of IRRDR ≥6 and age <60 years improved SVR predictability (93.3 %), and that of IRRDR ≤5 and age ≥60 years improved non-SVR predictability (84.0 %). Similarly, a combination of IL28B minor and platelets <15 × 10(4)/mm(3) improved NVR predictability (85.7 %), and that of IL28B major and platelets ≥15 × 10(4)/mm(3) improved non-NVR (response) (97.1 %) predictability. CONCLUSION: IRRDR ≥6 and age <60 years were significantly associated with SVR. IL28B minor and platelets <15 × 10(4)/mm(3) were significantly associated with NVR. Certain combinations of these factors improved SVR and NVR predictability and could, therefore, be used to design therapeutic strategies.


Assuntos
Antivirais/uso terapêutico , Hepacivirus/genética , Hepatite C Crônica/tratamento farmacológico , Interferon-alfa/uso terapêutico , Interleucinas/genética , Ribavirina/uso terapêutico , Adulto , Idoso , Antivirais/administração & dosagem , Quimioterapia Combinada , Feminino , Genótipo , Hepatite C Crônica/genética , Hepatite C Crônica/virologia , Humanos , Interferon-alfa/administração & dosagem , Interferons , Modelos Logísticos , Masculino , Pessoa de Meia-Idade , Mutação , Polimorfismo Genético , Ribavirina/administração & dosagem , Análise de Sequência , Resultado do Tratamento , Carga Viral , Proteínas não Estruturais Virais
8.
Intervirology ; 55(1): 1-11, 2012.
Artigo em Inglês | MEDLINE | ID: mdl-21293098

RESUMO

OBJECTIVE: Hepatitis C virus (HCV genome) polymorphisms are thought to influence the outcome of pegylated-interferon/ribavirin (PEG-IFN/RBV) therapy. This study aimed to examine non-structural protein 5A (NS5A) polymorphisms, e.g. IFN/RBV resistance-determining region (IRRDR) and IFN sensitivity-determining region (ISDR), and core protein polymorphism as predictive therapeutic markers. METHODS: Pretreatment sequences of NS5A and core regions were analyzed in 68 HCV-1b-infected patients treated with PEG-IFN/RBV. RESULTS: Of 24 patients infected withHCV having an IRRDR with 6 or more mutations (IRRDR≥6), 18 (75%) patients achieved sustained virological response (SVR), whereas only 11 (25%) of 44 patients infected with HCV having IRRDR≤5 did. IRRDR≥6 was significantly associated with SVR (p < 0.0001). On the other hand, ISDR≥2 was significantly associated with relapse (either before [breakthrough] or after end-of-treatment response [ETR[-]relapse]) (p < 0.05) and a point mutation of the core protein from Arg to Gln at position 70 (Gln(70)) was significantly associated with null-response (p < 0.05). Multivariate analysis identified IRRDR≥6 as the only viral genetic factor that independently predicted SVR. CONCLUSION: NS5A (IRRDR and ISDR) and core protein polymorphisms are associated with the outcome of PEG-IFN/RBV therapy for chronic hepatitis C. In particular, IRRDR≥6 is a useful marker for prediction of SVR.


Assuntos
Hepatite C Crônica/tratamento farmacológico , Hepatite C Crônica/virologia , Interferon-alfa/administração & dosagem , Polietilenoglicóis/administração & dosagem , Polimorfismo Genético , Ribavirina/administração & dosagem , Proteínas do Core Viral/genética , Proteínas não Estruturais Virais/genética , Idoso , Sequência de Aminoácidos , Substituição de Aminoácidos , Antivirais/administração & dosagem , Feminino , Hepacivirus/genética , Hepacivirus/isolamento & purificação , Humanos , Interferon alfa-2 , Masculino , Pessoa de Meia-Idade , Dados de Sequência Molecular , Mutação de Sentido Incorreto , RNA Viral/genética , Proteínas Recombinantes/administração & dosagem , Análise de Sequência de DNA , Resultado do Tratamento
9.
J Virol ; 85(17): 8556-68, 2011 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-21697492

RESUMO

Chronic hepatitis C virus (HCV) infection is often associated with type 2 diabetes. However, the precise mechanism underlying this association is still unclear. Here, using Huh-7.5 cells either harboring HCV-1b RNA replicons or infected with HCV-2a, we showed that HCV transcriptionally upregulated the genes for phosphoenolpyruvate carboxykinase (PEPCK) and glucose 6-phosphatase (G6Pase), the rate-limiting enzymes for hepatic gluconeogenesis. In this way, HCV enhanced the cellular production of glucose 6-phosphate (G6P) and glucose. PEPCK and G6Pase gene expressions are controlled by the transcription factor forkhead box O1 (FoxO1). We observed that although neither the mRNA levels nor the protein levels of FoxO1 expression were affected by HCV, the level of phosphorylation of FoxO1 at Ser319 was markedly diminished in HCV-infected cells compared to the control cells, resulting in an increased nuclear accumulation of FoxO1, which is essential for sustaining its transcriptional activity. It was unlikely that the decreased level of FoxO1 phosphorylation was mediated through Akt inactivation, as we observed an increased phosphorylation of Akt at Ser473 in HCV-infected cells compared to control cells. By using specific inhibitors of c-Jun N-terminal kinase (JNK) and reactive oxygen species (ROS), we demonstrated that HCV infection induced JNK activation via increased mitochondrial ROS production, resulting in decreased FoxO1 phosphorylation, FoxO1 nuclear accumulation, and, eventually, increased glucose production. We also found that HCV NS5A mediated increased ROS production and JNK activation, which is directly linked with the FoxO1-dependent increased gluconeogenesis. Taken together, these observations suggest that HCV promotes hepatic gluconeogenesis through an NS5A-mediated, FoxO1-dependent pathway.


Assuntos
Fatores de Transcrição Forkhead/metabolismo , Gluconeogênese , Hepacivirus/patogenicidade , Interações Hospedeiro-Patógeno , Proteínas não Estruturais Virais/metabolismo , Linhagem Celular , Núcleo Celular/química , Proteína Forkhead Box O1 , Perfilação da Expressão Gênica , Glucose/metabolismo , Glucose-6-Fosfato/metabolismo , Hepatócitos/metabolismo , Hepatócitos/virologia , Humanos , Fosforilação , Mapeamento de Interação de Proteínas
10.
Microbiol Immunol ; 55(6): 418-26, 2011 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-21371092

RESUMO

Both host and viral factors have been implicated in influencing the response to pegylated-interferon/ribavirin (PEG-IFN/RBV) therapy for hepatitis C virus (HCV) infection. Among the viral factors, sequence heterogeneity within NS5A and core regions has been proposed. This study aimed to clarify the relationship between virological responses to PEG-IFN/RBV therapy and sequence heterogeneity within NS5A, including the IFN/RBV resistance-determining region (IRRDR), the interferon sensitivity-determining region (ISDR) and the core region. Pretreatment sequences of NS5A and the core regions were analyzed in 57 HCV-1b-infected patients who were to be treated with PEG-IFN/RBV. Of 40 patients infected with HCV having an IRRDR with four or more mutations (IRRDR ≥ 4), 28 (70%) patients achieved a sustained virological response (SVR). On the other hand, only 4 (24%) of 17 patients infected with HCV having an IRRDR with three or fewer mutations (IRRDR ≤ 3) achieved a SVR (P = 0.001). Similarly, 22 (71%) of 31 patients infected with HCV and having an ISDR with one or more mutations (ISDR ≥ 1) achieved a SVR while 10 (38%) of 26 patients infected with HCV and having an ISDR without any mutations (ISDR = 0) achieved a SVR (P = 0.014). As for the core region, there was significant correlation between a single mutation at position 70 (Gln(70) ) and non-SVR (P = 0.02). Notably, Gln(70) was more prominently associated with the null response (P = 0.0007). In conclusion, sequence heterogeneity within the IRRDR and ISDR, and a single point mutation at position 70 of the core region of HCV-1b are likely to be correlated with virological responses to PEG-IFN/RBV therapy.


Assuntos
Variação Genética , Hepacivirus/efeitos dos fármacos , Hepatite C/virologia , Interferons/administração & dosagem , Ribavirina/administração & dosagem , Proteínas do Core Viral/genética , Proteínas não Estruturais Virais/genética , Adulto , Idoso , Antivirais/administração & dosagem , Antivirais/farmacologia , Quimioterapia Combinada/métodos , Feminino , Hepacivirus/genética , Hepatite C/tratamento farmacológico , Humanos , Interferons/farmacologia , Masculino , Pessoa de Meia-Idade , Dados de Sequência Molecular , RNA Viral/sangue , RNA Viral/genética , Ribavirina/farmacologia , Análise de Sequência de DNA , Resultado do Tratamento , Carga Viral
11.
Microbiol Immunol ; 54(11): 684-90, 2010 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-21044142

RESUMO

Persistent infection with hepatitis C virus causes serious liver diseases, such as chronic hepatitis, hepatic cirrhosis and hepatocellular carcinoma. The male gender is one of the critical factors in progression of hepatic fibrosis due to chronic HCV infection; thus female hormones may play a role in delaying the progression of hepatic fibrosis. It has also been reported that women are more likely than men to clear HCV in the acute phase of infection. These observations lead the present authors to the question: do female hormones inhibit HCV infection? In this study using HCV J6/JFH1 and Huh-7.5 cells, the possible inhibitory effect(s) of female hormones such as 17ß-estradiol (the most potent physiological estrogen) and progesterone on HCV RNA replication, HCV protein synthesis and production of HCV infectious particles (virions) were analyzed. It was found that E2, but not P4, significantly inhibited production of the HCV virion without inhibiting HCV RNA replication or HCV protein synthesis. E2-mediated inhibition of HCV virion production was abolished by a nuclear estrogen receptor (ER) antagonist ICI182780. Moreover, treatment with the ERα-selective agonist 4, 4', 4″- (4-propyl-[1H]-pyrazole-1, 3, 5-triyl)trisphenol (PPT), but not with the ERß-selective agonist 2, 3-bis (4-hydroxyphenyl)-propionitrile (DPN) or the G protein-coupled receptor 30 (GPR30)-selective agonist 1-(4-[6-bromobenzo 1, 3 dioxol-5-yl]-3a, 4, 5, 9b-tetrahydro-3H-cyclopenta [c] quinolin-8-yl)-ethanone (G-1), significantly inhibited HCV virion production. Taken together, the present results suggest that the most potent physiological estrogen, E2, inhibits the production of HCV infectious particles in an ERα-dependent manner.


Assuntos
Estradiol/farmacologia , Hepacivirus/efeitos dos fármacos , Vírion/efeitos dos fármacos , Linhagem Celular Tumoral , DNA Viral/biossíntese , Estradiol/análogos & derivados , Receptor alfa de Estrogênio/fisiologia , Fulvestranto , Hepacivirus/fisiologia , Humanos , Nitrilas/farmacologia , Fenóis , Pirazóis/farmacologia , Proteínas Virais/biossíntese , Vírion/fisiologia
12.
Microbes Infect ; 11(4): 467-75, 2009 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-19397874

RESUMO

Subacute sclerosing panencephalitis (SSPE) is caused by variants of wild-type measles virus (MV). Such MV variants lack almost completely the ability to produce cell-free progeny virus. We recently isolated an MV variant that has only three amino acid mutations (L165P,L250P and Y282H) in the M protein compared with MV field isolates of the same genotype. In the present study, we analyzed the significance of these mutations with regard to the characteristics of the M protein and progeny virus production. We found that each of the three mutations rendered the M protein insoluble in 0.5% Triton X-100 and altered its subcellular localization, either when ectopically expressed alone using a plasmid-based expression system or when expressed in the context of viral replication. Moreover, each of the three mutations markedly, but not completely, impaired the ability of MV to produce cell-free progeny virus, with the degree of impairment being the same as for all three mutations together. These results suggest the possibility that the changes in the solubility and subcellular localization of the M protein determine the ability to produce cell-free progeny virus, at least to some extent, and play a role in the pathogenicity of variants causing SSPE.


Assuntos
Vírus do Sarampo/genética , Mutação de Sentido Incorreto , Mutação Puntual , Panencefalite Esclerosante Subaguda/virologia , Proteínas Virais/química , Proteínas Virais/genética , Replicação Viral , Substituição de Aminoácidos/genética , Animais , Núcleo Celular/química , Chlorocebus aethiops , Citoplasma/química , Humanos , Vírus do Sarampo/isolamento & purificação , Vírus do Sarampo/fisiologia , Solubilidade , Células Vero
13.
J Gen Virol ; 90(Pt 7): 1681-1691, 2009 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-19282429

RESUMO

Robust production of infectious hepatitis C virus (HCV) in cell culture was realized by using the JFH1 strain and the homologous chimeric J6/JFH1 strain in Huh-7.5 cells, a highly HCV-permissive subclone of Huh-7 cells. In this study, we aimed to establish a more efficient HCV-production system and to gain some insight into the adaptation mechanisms of efficient HCV production. By serial passaging of J6/JFH1-infected Huh-7.5 cells, we obtained culture-adapted J6/JFH1 variants, designated P-27, P-38 and P-47. Sequence analyses revealed that the adaptive mutant viruses P-27, P-38 and P-47 possessed eight mutations [four in E2, two in NS2, one in NS5A and one in NS5B), 10 mutations [two additional mutations in the 5'-untranslated region (5'-UTR) and core] and 11 mutations (three additional mutations in 5'-UTR, core and NS5B), respectively. We introduced amino acid substitutions into the wild-type J6/JFH1 clone, generated recombinant viruses with adaptive mutations and analysed their infectivity and ability to produce infectious viruses. The viruses with the adaptive mutations exhibited higher expression of HCV proteins than did the wild type in Huh-7.5 cells. Moreover, we provide evidence suggesting that the mutation N534H in the E2 glycoprotein of the mutant viruses conferred an advantage at the entry level. We thus demonstrate that an efficient HCV-production system could be obtained by introducing adaptive mutations into the J6/JFH1 genome. The J6/JFH1-derived mutant viruses presented here would be a good tool for producing HCV particles with enhanced infectivity and for studying the molecular mechanism of HCV entry.


Assuntos
Hepacivirus/crescimento & desenvolvimento , Hepacivirus/genética , Hepatócitos/virologia , Mutação , Regiões 5' não Traduzidas , Adaptação Biológica , Linhagem Celular Tumoral , Análise Mutacional de DNA , Humanos , Mutação de Sentido Incorreto , Mutação Puntual , Análise de Sequência de DNA , Inoculações Seriadas , Proteínas do Envelope Viral/genética , Proteínas não Estruturais Virais/genética
14.
J Hepatol ; 50(5): 883-94, 2009 May.
Artigo em Inglês | MEDLINE | ID: mdl-19303158

RESUMO

BACKGROUND/AIMS: Persistent infection with hepatitis C virus (HCV) causes extrahepatic diseases, including diabetes. We investigated the possible effect(s) of HCV replication on cellular glucose uptake and expression of the facilitative glucose transporter (GLUT) 2 and 1. METHODS: We used Huh-7.5 cells harboring either an HCV subgenomic RNA replicon (SGR) or an HCV full-genomic RNA replicon (FGR), HCV-infected cells, and the respective cells treated with interferon (IFN). We also used liver tissue samples obtained from patients with or without HCV infection. RESULTS: Glucose uptake and surface expression of GLUT2 and GLUT1 were suppressed in SGR, FGR and HCV-infected cells compared to the control cells. Expression levels of GLUT2 mRNA, but not GLUT1 mRNA, were lower in SGR, FGR and HCV-infected cells than in the control. Luciferase reporter assay demonstrated decreased GLUT2 promoter activities in SGR, FGR and HCV-infected cells. IFN treatment restored glucose uptake, GLUT2 surface expression, GLUT2 mRNA expression and GLUT2 promoter activities. Also, GLUT2 expression was reduced in hepatocytes of liver tissues obtained from HCV-infected patients. CONCLUSIONS: HCV replication down-regulates cell surface expression of GLUT2 partly at the transcriptional level, and possibly at the intracellular trafficking level as suggested for GLUT1, thereby lowering glucose uptake by hepatocytes.


Assuntos
Transportador de Glucose Tipo 1/metabolismo , Transportador de Glucose Tipo 2/metabolismo , Glucose/metabolismo , Hepacivirus/fisiologia , Fígado/metabolismo , Fígado/virologia , Replicação Viral/fisiologia , Antivirais/farmacologia , Carcinoma Hepatocelular/metabolismo , Carcinoma Hepatocelular/patologia , Carcinoma Hepatocelular/virologia , Linhagem Celular Tumoral , Regulação para Baixo/fisiologia , Hepatite C Crônica/metabolismo , Hepatite C Crônica/patologia , Hepatite C Crônica/virologia , Hepatócitos/efeitos dos fármacos , Hepatócitos/metabolismo , Hepatócitos/virologia , Humanos , Interferons/farmacologia , Fígado/citologia , Neoplasias Hepáticas/metabolismo , Neoplasias Hepáticas/patologia , Neoplasias Hepáticas/virologia , RNA Viral/metabolismo , Replicon , Transdução de Sinais/fisiologia
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