There is again no mention of non-migraine headaches. Eight treatment subjects experienced no significant change (12%). The subjects who proceeded with surgery experienced multiple complications that were present at 5-year follow-up. These complications included 20 subjects with occasional itching, 3 subjects had hair thinning at the surgical site, 2 subjects had hypersensitivity (frontal),

2 subjects had hyposensitivity (frontal), 2 subjects had numbness (frontal), and 3 subjects had mild occipital stiffness or weakness. One subject had facial nerve injury with complete recovery. The author specifically notes that no subjects had persistent intense itching Gemcitabine at 5 years, which leaves the possibility that some degree of itching at the surgical site may have been present. The authors report that among the 69 subjects in the final analysis, 61 had improvement of their headaches at the 5-year follow-up evaluation.

The author then comments that a placebo effect is highly unlikely in these subjects that have been followed OTX015 clinical trial over 5 years. It is then noted that in other studies, a positive response rate (reduction by 50%) of over 90% and a migraine elimination rate of over 70% is noted throughout the literature. The author then remarks that better detection and deactivation of trigger sites, as well as improving surgical techniques, may improve these success rates. The author specifically notes that resection of the temporal artery can be considered

in cases involving the auriculotemporal branch of the trigeminal nerve. Regarding the lesser occipital nerve, the author advocates neurectomy and “burying the tied end of the nerve in the adjacent muscle” followed by triamcinolone injection to avoid neuroma formation. These additional surgical techniques are based on little evidence. Commentary is then made about Acetophenone rebound headache, and subjects taking opiates, which is the only time the author comments on medications that are taken during the study. It is not surprising that the only medications noted by the author are those that may negatively impact study results (medication overuse headache), as there is no mention of preventative and abortive medications that can positively impact statistical analysis. The author once again lumps together these 4 procedures, and uses this collective weak data to reinforce these self-promoting curative surgical interventions. The improvement of a patient’s pain with nerve blocks or BTX could be used to persuade a patient to proceed with an expensive surgical treatment with unclear benefit and potentially irreversible complications including worsening of pain.

ChIP analysis demonstrated that PPARβ/δ directly bound to the promoter of genes including ANGPTL4, MTIF, and CITED2. Conclusions: PPARβ/δ appears to be Epigenetics inhibitor a functional tumor suppressor exerting an inhibitory effect on HCC growth in vitro and in vivo, and involved in liver carcinogenesis through direct and indirect regulation of tumor related genes. Thus PPARβ/δ is a target for the prevention and treatment of liver cancer. Disclosures: The following people have nothing to disclose: Bo Shen, Ai min Li, Yu Qiang Nie, Yu-Jui Yvonne

Wan, Yan Lei Du, Yu Yuan Li, Gui Jia Shen Background & Aims: Recent whole-genome sequencing (WGS) studies have uncovered many mutated genes in hepatocellu-lar carcinoma (HCC) tissues. These results seem reasonable given the important functional roles of these genes. On the other hand, host genetic factors associated with hepatocarcino-genesis have been intensively investigated by genome-wide association studies (GWAS) using germline DNA of patients. Several promising genes which are responsible for hepatocar-cinogenesis have been reported, such as KIF1B, MICA and DEPDC5, LBH589 but these genes are not identified as “frequently mutated genes“ in WGS studies, nor vice versa. We aimed to clarify the contribution of the genes, which have been detected by recent WGS studies, towards hepatitis C virus (HCV)-related hepatocarcinogenesis. Methods:

We reviewed recent WGS studies and selected several frequently mutated genes. Next, we selected single

nucleotide polymorphisms (SNPs) which have potential regulatory effects on expression levels of these candidate genes using available expression quantitative trait locus (eQTL) data from a public database that includes over 5,000 individuals. 11 SNPs were selected with sufficient statistical significance to overcome the lack of statistical power resulted from multiple testing in GWAS. Finally, we conducted Cell press a case-control analysis of these SNPs or SNPs linked to them (r2 > 0.8 in both European and Asian populations) using our previous GWAS data consisting of 212 chronic HCV carriers with HCC (cases) and 765 chronic HCV carriers without HCC (controls). Results: Among 11 SNPs selected, 8 SNPs showed cis-acting effects (i.e., the SNP is located near the expressed gene) on expression levels of frequently mutated genes; 5 for chromatin regulators, 3 for Wnt/beta-catenin signaling pathways, and 1 for a tumor suppressor. The two remaining SNPs showed trans-acting effects (i.e., the SNP is located far from the expressed gene or on another chromosome) on expression levels of 2 chromatin regulators. We successfully extracted genotyping data of 7 SNPs except for 4 SNPs which were not available in our GWAS platform. Finally, we analyzed the association between these SNP genotypes and development of HCC using various genetic models, but could not find any significant association (P > 0.05).

Immunoblot analysis showed J7-DKK4 cells secreted more DKK4 into the culture medium than did J7-control cells (Fig.

4A). The overexpression of DKK4 was significantly decreased cellular proliferation compared with J7-control cells (Fig. 4B). To test the effect of the DKK4 gene on cell invasiveness was measured in vitro using Matrigel Transwell invasion assays. Further, the AG-14699 invasiveness of J7-DKK4#1 and #2 cells was inhibited by 75%-80% in J7 cells (Fig. 4C). Images of cell density were shown for two control and two overexpressing cell lines (Fig. 4C). The quantified results are shown in Supporting Fig. 2A. To determine the effect of DKK4 on the Wnt-canonical signaling pathway, the expression of several proteins involved in this pathway was measured in J7 cells. β-Catenin was significantly down-regulated by 35%-40% in the two DKK4-overexpressing cell lines compared with control cell lines. In contrast, phosphorylated β-catenin protein was up-regulated by almost 1.6-fold in

the two DKK4-overexpressing cell lines. The expression levels of CD44, cyclin D1, and c-Jun significantly decreased in DKK4-overexpressing cell lines in immunoblot analysis (Fig. 4D; Supporting Fig. 2B). This is consistent Metabolism inhibitor with a previous study indicating that c-Jun is a target gene of the Wnt/β-catenin pathway in human colorectal carcinomas.18 Overexpression of DKK4 decreased the activity of pro-matrix metallopeptidase (pro-MMP)-9 (92 kDa) and pro-MMP-2 (72 kDa) by 65%-70% and 18%-30% in J7 cells, respectively (Fig. 4E; Supporting Fig. 2C). To confirm the effect of DKK4 on β-catenin-ubiquitin complex formation, we performed immunoprecipitation assays. The data indicate the DKK4-mediated ubiquitination of β-catenin

is involved in the degradation of β-catenin (Fig. 4F). To investigate the effect of DKK4 and TR on tumor growth in vivo, we established a xenograft of J7 cells in BALB/c nude mice. Three J7 isogenic cell lines, J7-control, J7-DKK4, and J7-TRα1 were established. To verify the levels of expression of the DKK4 and TR proteins in the three J7 cell lines, cells were incubated with 1 nM T3 for 24 hours. The levels of the DKK4 protein were increased in J7-DKK4 selleck and J7-TRα1 cells compared with J7-control cells (Fig. 5A). The three J7 cell lines were injected subcutaneously and monitored continuously for 21 days. Figure 4B shows the average tumor volume observed in each of the three groups (n = 4). J7-DKK4 and J7-TRα1-induced tumors grew significantly slower than did control tumors. On average, after 21 days, tumors detected in mice injected with J7-DKK4 and J7-TRα1 cells were 45%-90% smaller compared with the tumors observed in control mice (Fig. 5B). To determine whether the in vitro results (Fig. 4C) could be reproduced in vivo, we investigated the effect of DKK4 on lung colony-forming ability in SCID mice (Fig. 5C).

Most Australian Paediatric centres still employ standard IFX infusions with little published data regarding rapid infusion protocols in paediatric practice. Aim: From a Tertiary Paediatric

IBD centre, we describe the practice and safety of rapid, 1 hour IFX infusion since implementing a rapid infusion policy in October 2011. Methods: Retrospective chart review of children diagnosed with Crohn’s Disease and fulfilling Australian criteria for Infliximab therapy attending the Royal MI-503 price Children’s Hospital, Brisbane from October 2011 to May 2013. The Rapid Infusion policy is to give the 3 Induction and 1st maintenance infusion in the standard fashion, increasing the rate to completion over 2.5 hours. All subsequent infusions, commencing with 5th infusion are given over 1 hour. Pre-medication (loratidine, hydrocortisone, paracetamol) is not routinely given, only after a documented infusion reaction. Results: 50 children have been treated using the rapid infusion policy and received 373 IFX infusions. No serious or anaphylactic reaction requiring adrenalin has been observed. 3 (6%) of children experienced a transfusion reaction (1 fever to 38oC; 1 mild temporary rash; 1 nausea) in 3/373 infusions (0.8%) but only during the first 3, induction, 2 hour infusions. No child experienced a transfusion reaction during subsequent rapid 1 hour infusions. Dabrafenib molecular weight Each child who experienced

a reaction has subsequently tolerated 1 hour rapid infusions, with premedication, without recurrence of transfusion reaction. There were no predictive factors for reaction. 50/50 children and their parents report satisfaction with the shorter duration infusion find more and shorter hospital stay. The Infusion centre has been able to increase

the number of children receiving Infliximab infusion at each session, improving timely access to scheduled therapy. Conclusions: This audit of practice confirms that the Rapid Infusion IFX protocol commencing at Infusion 5 and without routine pre-medication is safe, practical and well accepted by children and care-givers, improving patient acceptance and access to efficacious medication. Even faster infusions are described and safe in Adult practice and may provide further improvement in paediatric care and service delivery. (1) Donnellan FC et al. “Accelerated infliximab infusions are safe and well tolerated in patients with inflammatory bowel disease”. European Journal of Gastroenterology & Hepatology 2009:21(1):71–75 J KERR,1 A NAIR,2 R HINDS1,2 1Department of Paediatric Gastroenterology, Monash Children’s Hospital, Clayton, Victoria, Australia, 2Department of Paediatrics, Monash University, Clayton, Victoria, Australia Introduction: Infliximab (IFX) is commonly used in the management of children with Crohn’s disease (CD). IFX is used in Australia when there has been inadequate response to other treatments or in the presence of fistulising disease.

The initial daily dose of TVR (1500 or 2250 mg/day) and administration intervals (q8h or q12h) Cetuximab were determined by each attending physician according to age, sex,

bodyweight and hemoglobin level. Peginterferon-α-2b (PEG-Intron; MSD, Tokyo, Japan) was injected s.c. at a median dose of 1.5 μg/kg per week. Ribavirin (Rebetol; MSD) dose was adjusted according to bodyweight (600, 800 and 1000 mg for <60, ≥60 to <80, and ≥80 kg, respectively). In patients with hemoglobin level of less than 13 g/dL at the start of therapy, ribavirin dose was reduced by 200 mg in accordance with the general consensus statements.[28] Triple therapy was administrated for 12 weeks, followed by an additional 12 weeks of peginterferon-α-2b and ribavirin combination therapy (T12PR24) or 36 weeks of peginterferon-α-2b and ribavirin (T12PR48) in patients who agreed to the extended therapy. The administration of each drug was appropriately reduced or withdrawn if a serious adverse event occurred or was suspected to be developing during the course of treatment. Treatment was stopped for patients with HCV RNA of more than 3 log10 IU/mL at week 4, detectable HCV RNA at week 12 or a more

than 2 log10 IU/mL increase in HCV RNA levels from the lowest level during therapy irrespective of adverse events because of the low likelihood of achieving Cabozantinib an SVR and high likelihood of developing antiviral resistance. Virological response was analyzed on an intent-to-treat basis. The successful end-point of treatment was SVR for patients showing find more undetectable HCV RNA for 24 weeks after treatment cessation. Relapse was defined as when HCV RNA levels became undetectable by the end-of-treatment but became positive during the follow-up period. Viral breakthrough (VBT) was defined as when HCV RNA

became undetectable during the treatment period but then became positive before the end of the treatment period. Non-response was defined as when HCV RNA was detectable throughout the treatment period. Extended rapid virological response (eRVR) was defined as undetectable HCV RNA at both weeks 4 and 12 after starting treatment. All patients provided written informed consent. The study protocol conformed to ethics guidelines established in adherence with the 2008 Declaration of Helsinki and was approved by the ethics committee of each participating institution. Hepatitis C virus genotype was determined by direct sequencing followed by phylogenic analysis of the NS5B region.[29] The antiviral effects of therapy on HCV were assessed by measuring serum HCV RNA levels during treatment at least once every 4 weeks before, during and after therapy. HCV RNA levels were determined using the COBAS AmpliPrep/CABAS TaqMan HCV Test (Roche Diagnostics). The linear dynamic range of the assay was 1.2–7.8 log10 IU/mL, and undetectable samples were defined as negative. Core amino acid substitution at position 70 was determined as described previously.

Together with the presence of intermediate grey colour

expressed by intermediate-sized individuals, this fish could ontogenetically changes their body colour from white to black. Both sexes of black individuals selleck occupied feeding territories, but white individuals were non-territorial, indicating that the black body signals the possession of a feeding territory. Sexually active females were invariably black, whereas sexually active males were both black and white in colour. Few of the largest black males held harems, which included several female territories, whereas the remaining males were bachelors with no female territories. These bachelor males invested more in testes than harem males, suggesting that bachelors employ sneaking tactics, which is corroborated by our sneaking observations. To our knowledge, this is the first study showing that sneakers are entirely dissimilar to females in appearance. Herein,

we discuss why sneakers are dichromatic in relation to their life histories. “
“The chamois Rupicapra rupicapra has been termed a highly polygynous species, with a great male competition for mating. If so, a lower survival should be expected for the male sex. From 1986 to 2000, 1801 carcasses of chamois were collected in the Maritime Alps Regional Park, Italy, where a protected, healthy, stable population of chamois occurred (c. 12 individuals 100 ha−1). Each year, population structure from carcasses Selleckchem Alvelestat was consistent with that from the count carried out on the preceding year on live individuals. Demographic features (assessed from mortality data, as well as from live counts) showed a balanced age structure and a good adult survival (10% individuals older than 11 years). Mortality peaks showed a cyclic pattern of 3–4 years. Winter severity and local density affected survival, with no significant difference between sexes. The number of carcasses was dependent on the combination of snow depth and mean temperature, in winter. Both sexes showed nearly the same survivorship curves, with a quite similar life expectancy in the first year (males=6.8 years, females=7.0 years), and the same maximum age

at death (16 years), as it may be expected in a monomorphic, monogamous species. This is, however, a rare event selleck chemicals llc among polygynous species, with a high male competition for females and male juvenile dispersion, which normally affect male survival. The similar adult survival of the two sexes could be explained by comparable energetic costs and risks for reproduction, or through greater fat reserves put on by males, before the rut, which may lower their winter mortality. “
“Packard and colleagues investigate the prediction of the body mass of dinosaurs, using allometric models, advocating parameter estimation via direct optimization of a least-squares criterion on arithmetic axes rather than the conventional approach based on linear least-squares regression on logarithmic axes.

Recommendations: For treatment-experienced patients: 10. Re-treatment with boceprevir or telaprevir, together with peginterferon alfa and weight-based ribavirin, can be recommended for patients who had virological relapse or were partial responders after a

prior course of treatment with standard interferon alfa or peginterferon alfa and/or ribavirin (Class 1, Level A). Adverse events occurred more frequently in patients treated with PIs than in those treated with PegIFN and RBV therapy alone. In the BOC trials, anemia and dysgeusia were the most common adverse events, whereas in the TVR trials, rash, anemia, pruritus, nausea, and diarrhea developed more commonly among those who received TVR than who received SOC therapy.12, 16 In the phase 3 TVR trials, a rash of any severity was noted in 56% of patients who received a TVR-based regimen compared to 32% of those who received a PegIFN RG-7388 purchase and RBV regimen.16

The rash was typically eczematous and maculopapular in character, consistent with a drug-induced eruption. In most patients, the rash was mild to moderate in severity but was severe (involving >50% of the body surface area) in 4% of cases. The development of rash necessitated discontinuation of TVR in 6% and of the entire regimen in 1% of the cases. The Stevens Johnson Syndrome or Drug-Related Eruption with Systemic Symptoms (DRESS) occurred in <1% of subjects but at a higher frequency than generally observed for other drugs. The response of the rash to local or systemic treatment with corticosteroids Doramapimod price and oral antihistamines is uncertain. Pruritus, commonly but not always associated with rash, was noted in ∼50% of patients who received TVR therapy.16 Anemia developed among recipients of both PIs. Hemoglobin decreases below 10 g/dL (grade 2 toxicity) occurred in 49% of patients see more who received a BOC regimen compared to 29% of those who received the SOC regimen, whereas 9% had a hemoglobin decline of <8.5 g/dL (grade 3 toxicity).12 Among patients treated with T12PR, hemoglobin levels of <10 g/dL were observed

in 36% of patients compared to in 14% of patients who received SOC, and 9% had hemoglobin decreases to <8.5 g/dL.16 Because hematopoietic growth factors were not permitted during the TVR trials, there was a 5%-6% higher rate of treatment discontinuation among those who developed anemia than among those who did not. However, neither anemia nor RBV dose reduction adversely affected the SVR rate. Of note is that in the BOC trial, SVR rates in patients managed by RBV dose reduction alone were comparable to those in patients managed with erythropoietin therapy.23 Similarly, in the TVR trials, dose reduction of RBV had no effect on SVR rates, and therefore dose reduction should be the initial response to management of anemia.

Here, using state-of-the-art HCV cell culture systems and human liver

samples, we present evidence that hepatocyte Nox1 and Nox4 are prominent sources of ROS during complete HCV replication. In agreement with a recent report that JFH1 core does not localize to the mitochondria, we did not find a significant elevation of mitochondrial ROS or ATP depletion with JFH1.3 However, it is possible that the role of mitochondria in HCV-induced oxidative stress is more pronounced with certain viral genotypes or cell types. Previously, HCV core protein was suggested to reduce the cell’s ability to up-regulate its antioxidant defenses.1 However, hepatitis C patients have elevated levels of antioxidant genes, and JFH1 increased the GSH concentration in our study (Supporting selleck inhibitor Fig. 2B)1; thus, to what extent HCV interferes with the antioxidant defense mechanisms during complete viral replication remains Selleck Maraviroc to be further examined. In this study, our objective was not only to find the

source of ROS during complete HCV replication but also to find the source of superoxide for peroxynitrite generation that we predicted would occur near the cell nucleus. In agreement with this hypothesis, nitrotyrosine and Nox activity were increased in the JFH1-transfected cell nucleus, and this increase was attenuated with siRNAs to Nox. Also, although the relative amount of nuclear Nox4 versus cytoplasmic Nox4 tended to vary from one experiment to another, Nox4 was always at least partly nuclear and colocalized with lamin A/C, particularly in the presence of HCV. Furthermore, selleck compound HCV elevated the intracellular superoxide concentration, and Huh7 cells overexpressing Nox4 showed an increased superoxide level. These data do not completely rule out the possibility that Nox4 generates superoxide indirectly through another source (or other sources) of superoxide in the cell, and the significant effect that Nox1 siRNA had on nuclear nitrotyrosine could at least in

part be due to the uncoupling of nitric oxide synthase by peroxynitrite. Nevertheless, our data strongly indicate that Nox enzymes can elevate the intracellular superoxide concentration either directly or indirectly in the cell and lead to increased generation of peroxynitrite in the hepatocyte nucleus during HCV infection. Indeed, although Nox4 has recently been suggested to generate H2O2 rather than superoxide by virtue of the chemical mechanism involving a terminal electron transfer from the one electron–carrying heme B, Nox family proteins must generate superoxide first before the formation of secondary products.6 Thus, the reported inability to detect superoxide with some Nox/Duox enzymes is likely due to rapid dismutation of superoxide to form H2O2, which under some circumstances occurs more rapidly than the reaction with the superoxide-detecting probe.

Here, using state-of-the-art HCV cell culture systems and human liver

samples, we present evidence that hepatocyte Nox1 and Nox4 are prominent sources of ROS during complete HCV replication. In agreement with a recent report that JFH1 core does not localize to the mitochondria, we did not find a significant elevation of mitochondrial ROS or ATP depletion with JFH1.3 However, it is possible that the role of mitochondria in HCV-induced oxidative stress is more pronounced with certain viral genotypes or cell types. Previously, HCV core protein was suggested to reduce the cell’s ability to up-regulate its antioxidant defenses.1 However, hepatitis C patients have elevated levels of antioxidant genes, and JFH1 increased the GSH concentration in our study (Supporting Carfilzomib in vitro Fig. 2B)1; thus, to what extent HCV interferes with the antioxidant defense mechanisms during complete viral replication remains Talazoparib mouse to be further examined. In this study, our objective was not only to find the

source of ROS during complete HCV replication but also to find the source of superoxide for peroxynitrite generation that we predicted would occur near the cell nucleus. In agreement with this hypothesis, nitrotyrosine and Nox activity were increased in the JFH1-transfected cell nucleus, and this increase was attenuated with siRNAs to Nox. Also, although the relative amount of nuclear Nox4 versus cytoplasmic Nox4 tended to vary from one experiment to another, Nox4 was always at least partly nuclear and colocalized with lamin A/C, particularly in the presence of HCV. Furthermore, see more HCV elevated the intracellular superoxide concentration, and Huh7 cells overexpressing Nox4 showed an increased superoxide level. These data do not completely rule out the possibility that Nox4 generates superoxide indirectly through another source (or other sources) of superoxide in the cell, and the significant effect that Nox1 siRNA had on nuclear nitrotyrosine could at least in

part be due to the uncoupling of nitric oxide synthase by peroxynitrite. Nevertheless, our data strongly indicate that Nox enzymes can elevate the intracellular superoxide concentration either directly or indirectly in the cell and lead to increased generation of peroxynitrite in the hepatocyte nucleus during HCV infection. Indeed, although Nox4 has recently been suggested to generate H2O2 rather than superoxide by virtue of the chemical mechanism involving a terminal electron transfer from the one electron–carrying heme B, Nox family proteins must generate superoxide first before the formation of secondary products.6 Thus, the reported inability to detect superoxide with some Nox/Duox enzymes is likely due to rapid dismutation of superoxide to form H2O2, which under some circumstances occurs more rapidly than the reaction with the superoxide-detecting probe.

In AML-12 cells, ethanol increased total lipin-1 protein levels (Fig. 2A). We assessed the subcellular localization of lipin-1 in response to ethanol treatment in

AML-12 cells. AML-12 cells were cultured in the presence of ethanol, and extracts of these cells were fractionated into cytosol and nuclei, followed by western blotting analysis. The increase in endogenous lipin-1 protein induced by ethanol was observed strictly in the cytosolic fractions (Fig. 2B). Immunofluorescent staining of nuclei (4′,6-diamidino-2-phenylindole [DAPI] staining) and lipin-1 confirmed that endogenous lipin-1 was present predominantly in the cytoplasm (Fig. 2C). Furthermore, click here treatment with ethanol dramatically increased the intensity of lipin-1 staining in the cytoplasm, as compared to controls, suggesting an increase of lipin-1 protein expression. Cellular PAP activity was significantly induced by ethanol treatment, compared with the control, in AML-12 cells (Fig. 2D). Collectively, these results suggest that ethanol promotes lipin-1 cytoplasmic accumulation

and induces its PAP activity. The effect of ethanol on the development of steatosis in AML-12 cells was determined by measuring cellular triglyceride Acalabrutinib in vivo (TG) content with enzymatic assays using a triglyceride kit.14 There was a significant, concentration-dependent increase in TG content of cells exposed to ethanol (Supporting Fig. 2). Moreover, treatment with either 4-MP or cyanamide (Cya) essentially blocked the ability of ethanol to increase TG levels, indicating that ethanol metabolism is necessary for ethanol-mediated cellular lipid accumulation (Fig. 3A). To determine whether the increased lipin-1 induced by ethanol would affect cellular TG synthesis, we examined TG accumulation in AML-12 cells transfected with Lpin1 short interfering (siRNA) or control siRNA in response to ethanol exposure. Knocking down lipin-1 with Lpin1 siRNA largely eliminated the capacity of ethanol to induce TG accumulation (Fig. 3B). Note that lipin-1 protein

levels were decreased ∼70% after transfection with Lpin1 siRNA (Supporting Fig. 1B). These results suggest that ethanol metabolism increases lipin-1 enzymatic activity and, subsequently, promotes TG accumulation. SREBP-1 functions selleck inhibitor together with nuclear factor Y (NF-Y) to transactivate the LPIN1 promoter through sterol regulatory element (SRE) and NF-Y-binding sites.15 The effect of ethanol on the binding of acetylated histone H3/Lys9 (lysine 9), SREBP-1, or NF-Y to the Lpin1-SRE binding site was determined using chromatin immunoprecipitation (ChIP) assays. After chromatin had been cross-linked in control and ethanol-treated AML-12 cells, it was sheared by sonication. DNA-protein complexes were immunoprecipitated with antibodies directed against acetylated histone H3/Lys9, SREBP-1, or NF-Y.