g., student dormitories, military recruits). Second, although the Hepatitis C Follow-up Survey is nested within the NHANES, the data from the follow-up survey cannot be used to generate population estimates because of the small number of respondents and low response rate. Frequencies for some questions may be affected by differences in characteristics of respondents and nonrespondents. In addition, the small sample size limited our power to detect statistically significant differences between subgroups. Third, the data are self-reported and therefore subject

to the usual biases associated with such data (e.g., recall bias), including possibly not understanding questions learn more regarding medical information, such as whether they have had a particular medical procedure performed or what they were told by a healthcare provider. Finally, the sample consisted of persons who were positive for anti-HCV, whether currently infected or not; thus, treatment would not have been indicated in all those

who received an ROF letter—however, 91 of 115 with HCV-RNA results Selleck GPCR Compound Library available were HCV-RNA positive when tested during the NHANES, suggesting chronic infection. In summary, we report results for a sample of NHANES participants who responded to a follow-up survey after having tested positive for past or current HCV infection from 2001 through 2008, which, to our knowledge, is the only survey of such individuals to be conducted as part of a national population-based study. These data indicate that

fewer than half of those infected with HCV may be aware of their infection. The findings suggest that more intensive efforts are needed to identify and test those at risk for HCV infection and the need to educate patients and providers about appropriate interaction on prevention decisions and actions. “
“Hepatitis C virus (HCV) can affect immune cells and induce various kinds of immune-related diseases including pyoderma gangrenosum. We experienced a difficult-to-treat case of pyoderma gangrenosum-like lesions in a patient with HCV infection. The patient was treated with pegylated interferon (PEG IFN)-α-2b and ribavirin (RBV) therapy and achieved a sustained MCE公司 virological response. Before the eradication of HCV, the frequency of T-helper 17 cells was remarkably high in comparison to chronic hepatitis C patients without extrahepatic immune-related diseases. Moreover, we could detect negative and positive strand-specific HCV RNA in the CD19+ B lymphocytes and CD4+ T lymphocytes. However, after the eradication of HCV, the immunological status became normal and the pyoderma gangrenosum-like lesions became stable without immunosuppressive therapy. Here, we report a sequential immunological analysis during PEG IFN/RBV therapy and the beneficial effect of HCV eradication in difficult-to-treat pyoderma gangrenosum-like lesions.

g., student dormitories, military recruits). Second, although the Hepatitis C Follow-up Survey is nested within the NHANES, the data from the follow-up survey cannot be used to generate population estimates because of the small number of respondents and low response rate. Frequencies for some questions may be affected by differences in characteristics of respondents and nonrespondents. In addition, the small sample size limited our power to detect statistically significant differences between subgroups. Third, the data are self-reported and therefore subject

to the usual biases associated with such data (e.g., recall bias), including possibly not understanding questions Dorsomorphin regarding medical information, such as whether they have had a particular medical procedure performed or what they were told by a healthcare provider. Finally, the sample consisted of persons who were positive for anti-HCV, whether currently infected or not; thus, treatment would not have been indicated in all those

who received an ROF letter—however, 91 of 115 with HCV-RNA results selleck chemical available were HCV-RNA positive when tested during the NHANES, suggesting chronic infection. In summary, we report results for a sample of NHANES participants who responded to a follow-up survey after having tested positive for past or current HCV infection from 2001 through 2008, which, to our knowledge, is the only survey of such individuals to be conducted as part of a national population-based study. These data indicate that

fewer than half of those infected with HCV may be aware of their infection. The findings suggest that more intensive efforts are needed to identify and test those at risk for HCV infection and the need to educate patients and providers about appropriate interaction on prevention decisions and actions. “
“Hepatitis C virus (HCV) can affect immune cells and induce various kinds of immune-related diseases including pyoderma gangrenosum. We experienced a difficult-to-treat case of pyoderma gangrenosum-like lesions in a patient with HCV infection. The patient was treated with pegylated interferon (PEG IFN)-α-2b and ribavirin (RBV) therapy and achieved a sustained 上海皓元 virological response. Before the eradication of HCV, the frequency of T-helper 17 cells was remarkably high in comparison to chronic hepatitis C patients without extrahepatic immune-related diseases. Moreover, we could detect negative and positive strand-specific HCV RNA in the CD19+ B lymphocytes and CD4+ T lymphocytes. However, after the eradication of HCV, the immunological status became normal and the pyoderma gangrenosum-like lesions became stable without immunosuppressive therapy. Here, we report a sequential immunological analysis during PEG IFN/RBV therapy and the beneficial effect of HCV eradication in difficult-to-treat pyoderma gangrenosum-like lesions.

16 Indeed, we found that IA had a longer half-life than IFNα and exhibited hepatic tropism. Liver targeting was ascertained by pharmacokinetic and biodistribution studies and also by the more intense activation of hepatic ISGs when using pIA for liver transduction than when employing pIFN or pALF, despite the fact that albumin-IFNα has a longer half-life than IA. Unexpectedly, fusion of IFNα to

ApoA-I markedly changed OTX015 datasheet the biological properties of IFNα. Thus, experiments in murine fibroblasts showed that the cytotoxic effects of either HDL-IA or rIA were significantly lower than those of IFNα. Moreover, although IFNα induces activation-dependent cell death in T lymphocytes,19, 20 this effect is much lower Selleckchem PD0332991 with IA. Thus, IA facilitates lymphocyte proliferation in response to mitogens. These in vitro results are in accordance with data from in vivo killing assays where we found that the adjuvant efficacy of IA was far superior to that of IFNα. These findings indicate that the immunostimulatory properties of IA are not merely related to its persistence in circulation but rather to the fact that IA does not induce cell death in activated lymphocytes as does IFNα. In order to explore whether the interaction of IA with SR-BI

(the main ApoA-I receptor11) is required for its enhanced adjuvant activity, we performed in vivo killing assays after LacZ vaccination using as adjuvants pIA or pIFN in SR-BI+/−, SR-BI−/−, and wildtype mice. Our data showing that the adjuvant effect of IA was superior in wildtype animals but not in SR-BI−/− animals indicates that ligation of IA to SR-BI is needed for the fusion protein to display its potent immunostimulatory properties. The lower cytotoxic activity of IA compared to IFNα is also reflected by their different influence on hematopoiesis. One of the side effects of IFNα treatment is the development of leukopenia and thrombocytopenia, which limits its use in patients who already have diminished blood counts.8 In contrast to 上海皓元 IFNα, the administration of IA did not significantly reduce the number of platelets and only

caused a transient drop in leukocytes, which rapidly recovered. Moreover, the bone marrow progenitor compartment was induced to proliferate in the absence of significant modifications in the number of circulating leukocytes and platelets, suggesting that IA might stimulate myelo and thrombopoiesis. The safety of IA was also demonstrated in mice whose liver was transduced with an AAV vector encoding IA. No hematological or biochemical toxicity was found in these animals at day 30 after vector administration. The improvement of the pharmacological profile of IFNα resulting from its linkage to ApoA-I was not reproduced by fusion to other apolipoproteins present in HDLs. Anchoring IFNα to ApoF generated an unstable molecule which was not expressed.

16 Indeed, we found that IA had a longer half-life than IFNα and exhibited hepatic tropism. Liver targeting was ascertained by pharmacokinetic and biodistribution studies and also by the more intense activation of hepatic ISGs when using pIA for liver transduction than when employing pIFN or pALF, despite the fact that albumin-IFNα has a longer half-life than IA. Unexpectedly, fusion of IFNα to

ApoA-I markedly changed Dactolisib molecular weight the biological properties of IFNα. Thus, experiments in murine fibroblasts showed that the cytotoxic effects of either HDL-IA or rIA were significantly lower than those of IFNα. Moreover, although IFNα induces activation-dependent cell death in T lymphocytes,19, 20 this effect is much lower see more with IA. Thus, IA facilitates lymphocyte proliferation in response to mitogens. These in vitro results are in accordance with data from in vivo killing assays where we found that the adjuvant efficacy of IA was far superior to that of IFNα. These findings indicate that the immunostimulatory properties of IA are not merely related to its persistence in circulation but rather to the fact that IA does not induce cell death in activated lymphocytes as does IFNα. In order to explore whether the interaction of IA with SR-BI

(the main ApoA-I receptor11) is required for its enhanced adjuvant activity, we performed in vivo killing assays after LacZ vaccination using as adjuvants pIA or pIFN in SR-BI+/−, SR-BI−/−, and wildtype mice. Our data showing that the adjuvant effect of IA was superior in wildtype animals but not in SR-BI−/− animals indicates that ligation of IA to SR-BI is needed for the fusion protein to display its potent immunostimulatory properties. The lower cytotoxic activity of IA compared to IFNα is also reflected by their different influence on hematopoiesis. One of the side effects of IFNα treatment is the development of leukopenia and thrombocytopenia, which limits its use in patients who already have diminished blood counts.8 In contrast to MCE公司 IFNα, the administration of IA did not significantly reduce the number of platelets and only

caused a transient drop in leukocytes, which rapidly recovered. Moreover, the bone marrow progenitor compartment was induced to proliferate in the absence of significant modifications in the number of circulating leukocytes and platelets, suggesting that IA might stimulate myelo and thrombopoiesis. The safety of IA was also demonstrated in mice whose liver was transduced with an AAV vector encoding IA. No hematological or biochemical toxicity was found in these animals at day 30 after vector administration. The improvement of the pharmacological profile of IFNα resulting from its linkage to ApoA-I was not reproduced by fusion to other apolipoproteins present in HDLs. Anchoring IFNα to ApoF generated an unstable molecule which was not expressed.

16 Indeed, we found that IA had a longer half-life than IFNα and exhibited hepatic tropism. Liver targeting was ascertained by pharmacokinetic and biodistribution studies and also by the more intense activation of hepatic ISGs when using pIA for liver transduction than when employing pIFN or pALF, despite the fact that albumin-IFNα has a longer half-life than IA. Unexpectedly, fusion of IFNα to

ApoA-I markedly changed ABT-263 solubility dmso the biological properties of IFNα. Thus, experiments in murine fibroblasts showed that the cytotoxic effects of either HDL-IA or rIA were significantly lower than those of IFNα. Moreover, although IFNα induces activation-dependent cell death in T lymphocytes,19, 20 this effect is much lower selleck inhibitor with IA. Thus, IA facilitates lymphocyte proliferation in response to mitogens. These in vitro results are in accordance with data from in vivo killing assays where we found that the adjuvant efficacy of IA was far superior to that of IFNα. These findings indicate that the immunostimulatory properties of IA are not merely related to its persistence in circulation but rather to the fact that IA does not induce cell death in activated lymphocytes as does IFNα. In order to explore whether the interaction of IA with SR-BI

(the main ApoA-I receptor11) is required for its enhanced adjuvant activity, we performed in vivo killing assays after LacZ vaccination using as adjuvants pIA or pIFN in SR-BI+/−, SR-BI−/−, and wildtype mice. Our data showing that the adjuvant effect of IA was superior in wildtype animals but not in SR-BI−/− animals indicates that ligation of IA to SR-BI is needed for the fusion protein to display its potent immunostimulatory properties. The lower cytotoxic activity of IA compared to IFNα is also reflected by their different influence on hematopoiesis. One of the side effects of IFNα treatment is the development of leukopenia and thrombocytopenia, which limits its use in patients who already have diminished blood counts.8 In contrast to medchemexpress IFNα, the administration of IA did not significantly reduce the number of platelets and only

caused a transient drop in leukocytes, which rapidly recovered. Moreover, the bone marrow progenitor compartment was induced to proliferate in the absence of significant modifications in the number of circulating leukocytes and platelets, suggesting that IA might stimulate myelo and thrombopoiesis. The safety of IA was also demonstrated in mice whose liver was transduced with an AAV vector encoding IA. No hematological or biochemical toxicity was found in these animals at day 30 after vector administration. The improvement of the pharmacological profile of IFNα resulting from its linkage to ApoA-I was not reproduced by fusion to other apolipoproteins present in HDLs. Anchoring IFNα to ApoF generated an unstable molecule which was not expressed.

Recent studies have proved that molecules secreted from or shed from the surface of cancer cells were promising sources of potential serum cancer biomarkers. The aim of the present study was to identify putative secreted proteins capable of discriminate chemo-sensitive GC patients from chemo-resistant ones. Methods: The conditioned medium of two multidrug resistant gastric cell lines, SGC7901/ADR and SGC7901/VCR, and the parental SGC7901 cell line were analyzed

by MALDI-TOF/TOF mass spectrometry and the gene expression profile HKI-272 cell line were compared by cDNA array. The high throughput screening results were validated by qRT-PCR and western blot. Results: Comparative secretome analysis in combination with cDNA array assay totally identified 19 differentially secreted proteins between drug resistant and parental cell lines. In the subsequent verification by

qRT-PCR, twelve of the 19 proteins were found to be overexpressed in mRNA level in drug resistant cells, among which ADAM22, EFEMP1, TGFβ2, CGA and PROCR displayed the most distinguishable fold change and were chose for further analysis. Western blot results showed that all the five candidates were upregulated in both cell lysates and conditioned medium of the drug resistant cell lines. Conclusion: Through secretome analysis of two multidrug resistant gastric cell lines, we identified ADAM22, EFEMP1, TGFβ2, CGA and PROCR as putative biomarkers of AZD6244 MDR in GC. However, further validation in animal models as well as clinical samples is required before application in clinical settings. Key Word(s): 1. Stomach neoplasms; 2. Multidrug resistance; 3. Biomarkers; 4. Secretome; Presenting Author: RICARDO OLIVEIRA Additional Authors: GUSTAVO MOTA, GARDENIA COSTA, JOSESEBASTIAO

SANTOS Corresponding Author: RICARDO OLIVEIRA Affiliations: University of Sao Paulo Objective: Achalasia subtyping MCE公司 according Chicago criteria is helpful in guiding achalasia therapy. Several studies indicate that esophageal motor activity as demonstrated by HRM in healthy volunteers is affected by body posture. How body posture affects the results of HRM in achalasia is largely unknown. We compared the performance the Chicago criteria for achalasia subtyping on HRM plots in both the supine and sitting position. Methods: HRM was performed on 32 subjects with a diagnosis of achalasia classified as either Chagasic achalasia (CA, n = 13, 10 males, 35–73 years) or idiopathic achalasia (IA, n = 19; 8 males, 26–54 years) according the results of a serological complement fixation test for Chagas’ disease. HRM was performed using a solid state 32 sensor catheter system and a dedicated display software (Sandhill Instruments). The protocol comprised a baseline recording, ten 5 mL saline swallows sitting, and ten 5 mL saline swallows supine.

Recent studies have proved that molecules secreted from or shed from the surface of cancer cells were promising sources of potential serum cancer biomarkers. The aim of the present study was to identify putative secreted proteins capable of discriminate chemo-sensitive GC patients from chemo-resistant ones. Methods: The conditioned medium of two multidrug resistant gastric cell lines, SGC7901/ADR and SGC7901/VCR, and the parental SGC7901 cell line were analyzed

by MALDI-TOF/TOF mass spectrometry and the gene expression profile Doxorubicin were compared by cDNA array. The high throughput screening results were validated by qRT-PCR and western blot. Results: Comparative secretome analysis in combination with cDNA array assay totally identified 19 differentially secreted proteins between drug resistant and parental cell lines. In the subsequent verification by

qRT-PCR, twelve of the 19 proteins were found to be overexpressed in mRNA level in drug resistant cells, among which ADAM22, EFEMP1, TGFβ2, CGA and PROCR displayed the most distinguishable fold change and were chose for further analysis. Western blot results showed that all the five candidates were upregulated in both cell lysates and conditioned medium of the drug resistant cell lines. Conclusion: Through secretome analysis of two multidrug resistant gastric cell lines, we identified ADAM22, EFEMP1, TGFβ2, CGA and PROCR as putative biomarkers of CDK inhibitor MDR in GC. However, further validation in animal models as well as clinical samples is required before application in clinical settings. Key Word(s): 1. Stomach neoplasms; 2. Multidrug resistance; 3. Biomarkers; 4. Secretome; Presenting Author: RICARDO OLIVEIRA Additional Authors: GUSTAVO MOTA, GARDENIA COSTA, JOSESEBASTIAO

SANTOS Corresponding Author: RICARDO OLIVEIRA Affiliations: University of Sao Paulo Objective: Achalasia subtyping MCE according Chicago criteria is helpful in guiding achalasia therapy. Several studies indicate that esophageal motor activity as demonstrated by HRM in healthy volunteers is affected by body posture. How body posture affects the results of HRM in achalasia is largely unknown. We compared the performance the Chicago criteria for achalasia subtyping on HRM plots in both the supine and sitting position. Methods: HRM was performed on 32 subjects with a diagnosis of achalasia classified as either Chagasic achalasia (CA, n = 13, 10 males, 35–73 years) or idiopathic achalasia (IA, n = 19; 8 males, 26–54 years) according the results of a serological complement fixation test for Chagas’ disease. HRM was performed using a solid state 32 sensor catheter system and a dedicated display software (Sandhill Instruments). The protocol comprised a baseline recording, ten 5 mL saline swallows sitting, and ten 5 mL saline swallows supine.

Spd or Spm pretreatments reduced H2O2 accumulation and lipid peroxidation during 90‰ treatment and improved the recovery growth rate after transfer from 90‰ to 30‰. Increases in iron superoxide dismutase (FeSOD; EC 1.15.1.1) activity and

transcript levels observed under 90‰ were further increased by Spd and Spm pretreatments, while Put pretreatment had no effect. Increases in MnSOD activity and transcript levels observed under 90‰ were enhanced by Spd and Put pretreatment. An observed increase in catalase (CAT; EC 1.11.1.6) activity FK866 clinical trial and transcript levels under 90‰ was not affected by Spd and Spm pretreatments but was inhibited by Put pretreatment. Observed increases in ascorbate peroxidase (APX; EC 1.11.1.11) activity and transcript levels under 90‰ were inhibited by Put, Spd, and Spm pretreatments. In conclusion, Spd and Spm treatment affords U. fasciata protection against hypersalinity through the up-regulation of FeSOD gene expression, thereby alleviating oxidative damage. “
“The effects of QB-binding D1-protein mutations on the phenotypic characteristics and on hydrogen production of sulfur-deprived http://www.selleckchem.com/products/VX-809.html Chlamydomonas reinhardtii P. A. Dang. cultures were investigated. The mutation involved one (D240) or double (D239–40) amino-acid deletions at positions 240 and 239–240, respectively, in the loop connecting helices D and E of the D1 protein. Phenotypic characterization

of the mutants showed the following peculiarities as compared to the wildtype (WT): (i) a higher sensitivity to photoinhibition, (ii) a reduced amount of chl per dry weight and per cell, (iii) a higher respiration-to-photosynthesis ratio, (iv) a higher carbohydrate accumulation during the aerobic phase, and (v) a higher synthesis of xanthophyll-cycle pigments. These differences were translated into a 12- to 18-fold higher hydrogen biogas production. “
“In slow mainstream flows (<4–6 cm · s−1), the transport of dissolved nutrients to seaweed

blade surfaces is reduced due to the formation of thicker diffusion boundary layers (DBLs). The blade morphology MCE of Macrocystis pyrifera (L.) C. Agardh varies with the hydrodynamic environment in which it grows; wave-exposed blades are narrow and thick with small surface corrugations (1 mm tall), whereas wave-sheltered blades are wider and thinner with large (2–5 cm) edge undulations. Within the surface corrugations of wave-exposed blades, the DBL thickness, measured using an O2 micro-optode, ranged from 0.67 to 0.80 mm and did not vary with mainstream velocities between 0.8 and 4.5 cm · s−1. At the corrugation apex, DBL thickness decreased with increasing seawater velocity, from 0.4 mm at 0.8 cm · s−1 to being undetectable at 4.5 cm · s−1. Results show how the wave-exposed blades trap fluid within the corrugations at their surface. For wave-sheltered blades at 0.8 cm · s−1, a DBL thickness of 0.73 ± 0.

For example, patients with a platelet count <100,000/mm3 were PI3K inhibitor 11-fold more likely to experience a decompensation event and 14-fold more likely to die a liver-related death or undergo liver transplantation, compared with subjects with a baseline platelet count ≥200,000/mm3. Rates of outcomes were also evaluated according to baseline body mass index, ALT activity, and serum HCV RNA. The annualized rate of cirrhosis was 8.9% for nonobese subjects versus 11.3% for obese subjects (P = 0.07); 8.2% for ALT <90 IU/L versus 12.2% for ALT ≥90 IU/L

(P = 0.001); and 11.1% for HCV RNA <6.5 log10 IU/mL versus 9.0% for HCV RNA ≥6.5 log10 IU/mL (P = 0.046). Rate of any clinical outcome was not associated with baseline obesity or with ALT activity (P ≥ 0.30) but was associated with lower HCV RNA level (P < 0.0001). The association of outcomes with HCV Akt inhibitor RNA level was not adjusted for stage of fibrosis,

which was strongly and inversely associated with HCV RNA level (P < 0.0001). Understanding the natural history of advanced hepatitis C has been challenging. Limitations in study design or execution of most, if not all, prior studies could have led to inaccurate results. No prior study had the rigor of the histological evaluation of the HALT-C Trial, in which three liver biopsies were performed and each biopsy was assessed by a team of 11 expert liver histopathologists who were masked to all patient information.11, 12 Additionally, few if any prior studies had uniform monitoring of patients at regular intervals and predefined case definitions, whereas patients in the HALT-C Trial were evaluated every 3-6 months throughout the study, and all outcomes were reviewed independently by experienced hepatologists. Furthermore, all patients in the HALT-C Trial had failed to clear HCV during peginterferon and ribavirin therapy, whereas in several other studies, progression was evaluated in patient cohorts, only subsets of whom were treated, and in whom selection for therapy was not based on uniform criteria. For the HALT-C Trial, our hypothesis was that 3.5 years of maintenance, low-dose (90 μg/week) peginterferon therapy would retard the

progression of chronic hepatitis C in patients with advanced fibrosis; unfortunately, maintenance therapy was found to be ineffective. MCE Because clinical outcome rates were either indistinguishable between treated and control patients or were inconsistently different (higher mortality among treated patients with noncirrhotic fibrosis and lower incidence of HCC among treated patients with cirrhosis), we pooled the two groups for an analysis of the rate of progression of chronic hepatitis C. We followed the combined cohort of >1,000 patients with clinically compensated advanced fibrosis or cirrhosis, both during the randomized (maintenance versus control) phase and the postrandomization phase for up to 8 years (median, 5.6 years).

3C; Supporting Fig. 4), already described to be involved in HCC.[16] Remarkably, among the most dysregulated there was the NRF2-dependent pathway (Fig. 3C), whose role in cancer development has recently become a topic of an important controversy.[17] The finding that the majority of NRF2 target genes were up-regulated indicates MG-132 cell line activation of the NRF2 pathway (Fig. 3D). Notably, several of these genes were among the most up-regulated in both KRT-19+ lesions and aHCCs (see Table 1). Moreover, the small musculoaponeurotic fibrosarcoma oncogene homolog (MAF) family of transcription factors, which operate as coactivators

of NRF2,[18] was found activated at all stages of HCC development (Fig. 3C; Supporting Fig. 4). To identify a possible correlation between miRNAs and genes dysregulated at the initial stage of the process, we selected conserved putative miRNA targets in rat, predicted by the TargetScanS algorithm. For each of the differentially expressed genes in KRT-19+ nodules, we extracted the

annotated regulating miRNAs and performed an intersection with the differentially expressed miRNAs in the same stage. We found PD0332991 mouse that a consistent percentage of modified genes are targets of dysregulated miRNAs (Fig. 4). To study the relative expression of miRNAs and of their target genes, we evaluated the number of positive and negative correlations between the predicted miRNA-target gene pairs by means of the fold-change value reported by the Limma package. The results show that 171 out of 215 miRNA/mRNA pairs (79%) shown in Fig. 4 displayed anticorrelated expression, while 44 were positively correlated. In the transition from normal liver to KRT-19+ nodules we observed at least two relevant nodes, where two miRNA families, miR-30 and miR-200, control the expression of many modified medchemexpress genes. While expression of the miR-30 family was mainly modified at this

initial stage, miR-200 family was up-regulated in both preneoplastic lesions and aHCCs (Supporting Fig. 5). Notably, one of the target genes of miR-200a is kelch-like ECH-associated protein 1 (KEAP1), a negative regulator of NRF2.[19] NRF2 is an integrated redox sensitive signaling system that regulates 1%-10% of human genes and is negatively controlled by KEAP1, which promotes NRF2 proteasome-mediated degradation.[19] As mentioned above, the NRF2 pathway was already activated in early preneoplastic lesions and along tumor progression (Fig. 3C,D). Accordingly, immunohistochemistry (IHC) performed on lesions at different stages revealed that all of them were strongly positive for NRF2 (Fig. 5A); most important, IHC showed NRF2 nuclear staining in several preneoplastic and neoplastic hepatocytes, clearly demonstrating translocation and suggesting activation of this transcription factor.