WT and TGR5 KO mice had similar

body weights; however, KO mice had a significantly smaller liver/body-weight ratio (Fig. 1A,B). Hepatocyte size, analyzed on phalloidin-stained liver sections, was similar in WT and TGR5 KO mice (Supporting Fig. 1A). Hematoxylin and eosin (H&E) staining revealed normal liver histology in the majority ITF2357 price of WT and TGR5 KO mice, although approximately 20% of TGR5 KO mice exhibited mild portal inflammation and fibrosis (Supporting Fig. 1B). Basal biochemical blood parameters (alanine aminotransferase [ALT], alkaline phosphatase [ALP], bilirubin, total bile acids [TBA], glucose, and insulin concentrations) fell in the normal range in both genotypes (Supporting Table 2). After PH, TGR5

KO mice exhibited a significantly slower liver mass restoration (Fig. 1C and Supporting Fig. 2A,B) and a reduced mitotic activity, as compared to WT mice, especially at 2 and 3 days, whereas at later time points (days 5 and 9), there was a significant trend to compensate this deficit in TGR5 KO mice (Fig. 1D-F). A majority of TGR5 KO mice (60%-75%) exhibited jaundice as soon as 2-3 days after PH and recovered Gefitinib order afterwards. H&E staining after PH showed, exclusively in TGR5 KO mice, periportal patchy hepatocyte necrosis (Fig. 2A), increasingly extensive up to 72 hours, closely mimicking clusters of injured hepatocytes (“bile infarcts”) observed after BDL in mice.[20] At 5, 9, and 15 days afterwards PH, hepatocyte necrosis and inflammatory infiltrates progressively declined (data not shown), whereas periductular fibrosis appeared in a majority of TGR5 KO mice (day 15), but was lacking at day 21 (Supporting Fig. 2E). In WT mice, TBA raised immediately after PH in plasma,[3]

but also in liver during the first hours (Fig. 2B,C). Although this rise was transient in WT mice, massive and prolonged TBA accumulation in both plasma and liver was observed in TGR5 KO mice. No increase in post-PH mortality was noticed in TGR5 KO, as compared to WT mice (data not shown). The TGR5 KO phenotype could not be explained by a deficient hepatic adaptive response to post-PH BA overload, because Na+ taurocholate cotransporting polypeptide (NTCP), cholesterol 7α-hydroxylase (CYP7a1), organic solute transporter beta (OST-β), and bile salt export pump (BSEP) Resminostat messenger RNAs (mRNAs) were adequately regulated. This regulation was even stronger in TGR5 KO mice at days 3 and 5, when necroticoinflammatory injury and cholestasis were peaking, suggesting that FXR-dependent pathways were functional in those mice (Supporting Fig. 3E). In line with the fact that post-PH injury observed in TGR5 KO livers was suggestive of bile-induced toxicity,[20] we first observed that liver necrosis occurred very early on (4 hours) after PH in TGR5 KO mice, at a time when BA—in particular, hydrophobic BA—had already accumulated in liver (Supporting Fig. 4A-D).

The PG pathway is also involved in luminal bacterial sensing in the duodenum via activation of pattern recognition receptors, including Metabolism inhibitor Toll-like receptors and nucleotide-binding oligomerization domain 2. The presence of acute mucosal responses to luminal bacteria suggests that the duodenum is important for host defenses and may reduce bacterial loading to the hindgut using H2O2, complementing gastric acidity

and anti-bacterial bile acids. Prostaglandins (PGs) play a key role in mucosal defense, essential for maintaining the integrity of gastrointestinal (GI) tract. Nonsteroidal anti-inflammatory drugs (NSAIDs), through PG synthesis inhibition, injure the GI mucosa. In this review, we will discuss

how foregut chemosensors activate signaling pathways that enhance mucosal defense mechanisms via PG-related mechanisms. The duodenal mucosa, regularly exposed to gastric acid, and endogenous and exogenous chemicals including nutrients, has a unique luminal chemosensing capacity that enables the mucosa to sense luminal chemicals followed by rapid mucosal responses that protect the mucosa from injury, releasing mediators and hormones that have local and systemic effects.[1] The duodenal mucosa possesses three chemosensing modes (Fig. 1): (i) Luminal chemicals traverse epithelial cells, activating chemosensors expressed on subepithelial Pembrolizumab clinical trial afferent nerves (Fig. 1a). This pattern includes luminal CO2/H+ sensing and spice sensing. Luminal CO2 rather than H+ traverses apical membrane of villous cells and acidifies the cytoplasm due to carbonic anhydrase activity, followed by H+ extrusion through basolateral Na+/H+ exchanger-1, which activates transient receptor potential vanilloid-1 expressed on capsaicin-sensitive afferent nerves.[2, 3] Luminal capsaicin or the transient receptor potential (TRP) channel ankyrin-1 agonist also shares this pathway.[4, 5] (ii) Luminal chemicals activate apical chemoreceptors, followed by mediator release

from epithelial cells (Fig. 1b). Examples include luminal Decitabine in vitro ATP-P2Y signaling or acid-induced PG release, stimulating protective HCO3− and mucus secretion.[6, 7] (iii) Luminal chemicals activate G protein-coupled receptors expressed on enteroendocrine cells, followed by mediator or hormone release (Fig. 1c). Examples include luminal nutrient sensing by enteroendocrine cells. We have reported that luminal umami substances such as l-glutamate and 5′-inosine monophosphate activate taste receptors expressed on enteroendocrine L cells, which release the incretin glucagon-like peptide-1 and intestinotrophic glucagon-like peptide-2, the latter stimulating duodenal HCO3− secretion.

Small intestine is the most frequent site involved, accounting for 44% of all cases. It is most commonly diagnosed during childhood when complications such as gastrointestinal (GI) bleeding,

obstruction, or perforation occurred. Less than 30% cases are diagnosed in adults, and the diagnosis is mostly incidental. Methods: We report a case of a capsule endoscope lodged within an intestinal duplication. Results: A 61-year-old female was admitted to our hospital with a chief complaint of bloody stools for 2 days. Physical examination was unremarkable but laboratory tests revealed decreased hemoglobin (99 g/L) and positive fecal occult blood. Colonoscopy showed multiple diverticula in ascending colon, and a polyp of 0.3 cm in diameter in sigmoid colon. Gastroscopy Maraviroc molecular weight Dorsomorphin revealed nothing significant. Angiography demonstrated no active bleeding from the gastroduodenal artery and superior mesenteric artery. Therefore, the patient was diagnosed with obscure GI bleeding, and received capsule endoscopy (CE). CE revealed scattered erosions, superficial ulcers, and multiple diverticula in the small intestine (Figure 1). The capsule did not enter the colon at the end of examination and 10 days later. Then, single -balloon enteroscopy (SBE) was preformed to confirm the diagnosis and retrieve the capsule. SBE revealed an intestinal duplication in the middle part of ileum, and demonstrated

the capsule lodged in the duplication. The capsule was then safely retrieved using SBE (Figure 2). Conclusion: The patient declined surgical treatment. Fortunately, PIK3C2G her bleeding stopped spontaneously and has not recurred for over a year since discharge from hospital. Key Word(s): 1. duplication; 2. capsule endoscope; 3. enteroscopy; Presenting Author: YINGCHAO LI Additional Authors: SHUIXIANG HE Corresponding Author: YINGCHAO LI Affiliations: First affiliated hospital of medical college of Xi’an Jiaotong University Objective: To explore the safety and feasibility of endoscopic assisted laparoscopic resection of localized gastric gastrointestinal stromal tumors (GISTs). Methods: The clinical data for 55

patients who underwent resection of localized gastric GISTs by endoscopic assisted laparoscopic technique (27 cases) or pure laparoscopic technique (28 cases) in the First affiliated hospital of medical college of Xi’an Jiaotong University from 2010 to 2011 were analyzed retrospectively. The tumor size, tumor site, operative time, pathologic mitotic rate and immunohistochemical staining (CD117 and CD34), postoperative complication, recurrence and metastasis were compared between two groups. All patients underwent a routine follow-up for at least 1 year after the operation. Results: In gastric GISTs, the most common site of tumor is fundus of stomach. The operative time was 65 min ± 10 min and 82 min ± 14 min in the endoscopic assisted laparoscopy group and pure laparoscopy group respectively (P < 0.001).

Materials and Methods: レ4 consecutive patients with a diagnosis of fatty

liver disease who underwent a baseline TE examination between 2007 and 2010 at our Centre were genotyped for PNPLA3 rs734809 C/G, and investigated with a second TE examination at least 24 months apart. TE was considered reliable if >10 valid measurements were obtained, with selleck kinase inhibitor a success rate >65% and an interquartile range <30% of the result. Significant fibrosis was excluded by LSM <5.8 kPa as previously reported (Wong et al, Hepatology 2010). Results: Eleven (4%) patients had unsuccessful TE, 163 (108 men, 55 females) were included, 72% nonalcoholic fatty liver disease, 18% alcoholic liver disease, Talazoparib datasheet 19% diabetics, 34% with arterial hypertension, median age 52 yrs (range 18-73), BMI 27.5 kq/mq (range 1941), baseline LSM 6.3 kPa (range 2.5-63.9) and follow-up LSM 5.9 kPa (range 3.3-53.2), and interval between LSMs 41 months (range 24-76). At baseline 66 (41%) patients had LSM <5.8 kPa, 55% of them being PNPLA3 wild type compared to 34% of those with LSM >5.8 kPa (p=0.01).48 (29%) patients had both baseline and follow-up LSM <5.8 kPa, showing significantly lower baseline BMI (p<0.0001), higher baseline serum HDL (p=0.019) and lower triglycerides (p<0.0001) with respect to all other

patients. By multivariate logistic regression analysis PNPLA3 wild type (p=0.002, OR 3.1, 95%CI 2.1-11.5-6.4) and baseline triglycerides <120 mg/dl (p<0.0001, OR 4.4, 95%CI 2.1-9.1) independently predicted baseline LSM <5.8 kPa, conversely, BMI <29 kg/mq (p=0.003, OR 5.1, 95%CI 1.7-14.9) and triglycerides <120 mg/dl (p<0.0001, OR 4.6, 95%CI 2.1-10) independently predicted both baseline and follow-up LSM <5.8 for kPa. Conclusions:

Among patients with fatty liver, wild type PNPLA3 homozygosity and low serum triglycerides are independently associated with normal liver stiffness at presentation, but only the latter and being non-obese independently predict that they will maintain it during the follow-up. These results emphasize the role of modifiable risk factors in the progression of fatty liver. Disclosures: Mario Pirisi – Advisory Committees or Review Panels: Merck; Speaking and Teaching: Gilead, Bristol-Myers-Squibb The following people have nothing to disclose: Cristina Rigamonti, Michela E. Burlone, Miriam Gravellone, Andrea Magri, Rosalba Minisini, Cosimo Colletta Non-alcoholic fatty liver disease (NAFLD) has a complex natural history; only a fraction of patients progress to cirrhosis and its complications. Using paired biopsies one may detect gradual changes in fibrosis and other features prior to clinical cirrhosis.

S. revealed that hypertension was the only chronic physical condition that was specifically associated with migraine rather than headache in general.[49] Likewise, the association between migraine and obesity selleck chemicals has been shown to be attributable to headache in general rather than migraine,[103] whereas the association with migraine and cardiovascular disease is specifically associated with migraine. Similar

findings have emerged from studies of comorbidity in national samples of youth. In the first direct interview study that ascertained ICHD-II criteria for migraine in a nationally representative sample of U.S. adolescents, Lateef et al[50] found that allergies and asthma were specifically associated with migraine, whereas seizures and epilepsy were associated with headache in general. In contrast to research in adults, studies of comorbidity of headache/migraine in children have not demonstrated associations with either hypertension or cardiovascular disease in children. This suggests that cardiovascular risk factors and disorders may be a complication of migraine or an age-specific manifestation IWR-1 supplier of common etiologic factors. Prospective studies that elucidate the order of onset of migraine with respect

to comorbid disorders can provide clues regarding etiologic mechanisms. For example, Merikangas et al[104] demonstrated a prospective link between migraine and the incidence of stroke a decade later. This association has been subsequently replicated in numerous longitudinal studies.[105] Psychiatric comorbidity in migraine has also been well established in population samples of adults[51, 52, 69, 98] and children.[58, 64] Migraine is most strongly

associated with anxiety and mood disorders,[107] particularly phobic filipin states and major depression.[49] The presence of a pre-existing physical or medical disorder may also elevate the risk of migraine. Prospective research on children demonstrates that migraine is associated with an increased risk for the development of depression rather than the converse.[108] However, anxiety disorders, particularly phobias, are associated with an increased risk of migraine. This link may actually be a manifestation of underlying autonomic reactivity that may represent a common underlying diathesis for migraine. The elevated rates of infantile colic in children in treatment for migraine[109] would be consistent with this explanation. As such, comorbid disorders may reflect underlying etiologic rather than environmental triggers of migraine. Several studies have now confirmed that there is a syndromic association between migraine, depression, and anxiety, with anxiety preceding the onset of migraine followed by the subsequent development of mood disorders.

HCC is the most common primary malignant

tumor of the liver,34 and its incidence in PBC is not well known. Some studies have reported an increased risk of HCC in PBC patients, whereas others have found a low incidence of HCC in PBC. One reason for the controversy is that PBC is a relatively rare disease. Thus, the sample size was usually small in the majority of studies. For example, HCC was not found in PBC patients in the latest study by Ngu et al,27 though the investigators conceded that because the number of male PBC patients–the Crizotinib cost highest risk group for HCC—was so small (n = 6), it may have led to bias. The present meta-analysis, with a larger sample size and stronger evidence, demonstrated an increased risk of HCC in PBC patients, which was more than 18.8-fold higher than that of the general population. Another reason for the controversy is that there are some geographical and environmental differences between studies. Therefore, we further conducted subgroup meta-analyses,

which confirmed that this increased risk could not be affected by such variables as region (except the United States), age, sex, case ascertainment (except population-based studies), and type of effect size. However, there are still several confounding factors, such Sirolimus cell line as advanced histological stage (stage 4 PBC),1, 5, 8, 9, 21 history of blood transfusion,9, 28 and smoking or drinking habit,33–35 which might be associated with increased probability for HCC development in PBC patients or might be directly associated with PBC development. The interference of these factors cannot be excluded in this meta-analysis, because subgroup meta-analyses were not performed because of the small number of selected studies exploring the association of these factors with HCC risk in PBC patients. This might also be a major reason why there was significant heterogeneity between studies in overall meta-analysis

and in the majority of subgroup meta-analyses. Although the data on the association between PBC and the risks of stomach and pancreatic cancers are inconsistent, meta-analyses could not be conducted for assessing the association. The reason is that one study by Landgren et al,13 who found BCKDHB that PBC patients had increased risk of stomach cancer (RR, 1.66; 95% CI, 1.10-2.51) and pancreatic cancer (RR, 2.06; 95% CI, 1.44-2.96), examined the association only in male patients with PBC. However, other studies showing no significant association with the risks of these two cancers were performed in mixed-sex patient groups. Regardless, the present study suggests that the significant association between PBC and increased risk of stomach and pancreatic cancers cannot be excluded, at least not in male patients. A larger number of studies need to be performed to confirm this association. Notably, our present meta-analysis with insignificant between-study heterogeneity showed no significant association between PBC and breast cancer risk.

1999). Chronic effects of entanglement in free-swimming individuals include systemic infection and debilitation from extensive tissue damage (Cassoff et al. 2011). More common in protracted cases is severe

emaciation due to the inability to cope with a negative energy budget, driven by the combined effects of reduced mobility and foraging ability, and increased energetic demand imposed by towing accessory gear for months to years (Moore et al. 2006, Moore and van der Hoop 2012). Whereas disentanglement efforts were first developed to release Ipatasertib chemical structure large whales entangled and anchored in fixed fishing gear (Ledwell et al. 2010), techniques have been adapted to address the issue in free-swimming individuals (Moore et al. 2010). Disentanglement response efforts are coordinated by multiple agencies with the primary goal of removing all entangling gear. During a disentanglement procedure, buoys or floats are often added to trailing gear to increase a whale’s drag through the water and slow its movement (Moore et al. 2010). To further reduce boat aversion and allow for close approaches necessary for successful disentanglement, selleck chemicals methods have been developed to lightly sedate large whales

at sea (Moore et al. 2010). No data exist for large whales on the behavioral impacts of sedation and disentanglement or on the energetic cost of Ribose-5-phosphate isomerase entanglement in fishing gear due to drag. Through detailed

spatial and behavioral monitoring by means of a biologging tag (Dtag) (Johnson and Tyack 2003), we examined changes in dive behavior and kinematics of a tagged entangled North Atlantic right whale (North Atlantic Right Whale Catalog No. 3911, hereafter Eg 3911; Hamilton et al. 2007), before, during, and after disentanglement procedures on 15 January 2011. Further, we estimate drag forces experienced by the whale based on its body proportions, and the additional drag forces and energetic demand experienced while entangled in various gear configurations. Eg 3911, a female born in 2009 (NARWC Database, 2011), was first sighted entangled and displaying consequent emaciation on 25 December 2010 by an aerial survey team offshore Ponte Vedra Beach near Jacksonville, Florida. The entanglement involved attachment at a minimum of six sites around the mouth, wraps around both pectoral fins, and approximately 30 m of line trailing aft of the flukes (Moore et al. 2013) (Fig. 1). We conducted disentanglement attempts on 29 and 30 December 2010, though the whale remained entangled and was tracked by a satellite telemetry buoy. A third and final multiagency disentanglement effort took place 15 January 2011 near Melbourne, Florida, during which we tagged Eg 3911 with a biologging device (Dtag).

435, p < 0.0001). The retentive values of Efferdent, Listerine, Polident Overnight, and water were significantly higher than the retentive value of the attachments soaked in NaOCl. After 6 months of simulated use (548 pulls), the four denture cleansing find more solutions had significant effects on the retentive values of pink Locator attachments (F = 5.855, p = 0.003). The retentive values for attachments soaked in NaOCl (7.29 ± 1.0 N) were significantly lower than those of attachments soaked in Listerine (15.82 ± 4.7 N) and in Polident Overnight (14.41 ± 3.6 N). These cleansing solutions also had a significant effect on the percentage of retention lost (F = 3.271, p = 0.032). The

loss of retention in attachments soaked in Listerine (29 ± 9%) was significantly lower than attachments soaked in water (53 ± 12%). The loss

of retention in attachments soaked in Efferdent was 49 ± 9%; in Polident INK128 Overnight, 34 ± 18%; and in NaOCl, 42 ± 11%. There was no significant difference in the percentage of retention loss between water, Efferdent, NaOCl, and Polident Overnight. There was also no significant difference in the percentage of retention loss between Efferdent, NaOCl, Polident Overnight, and Listerine. Conclusion: NaOCl significantly decreased the retentive value of Locators. Therefore, it should not be routinely recommended for use as a denture cleanser. Listerine significantly increased the retention of the Locator attachments; however, it is premature to recommend Listerine for use as a denture cleanser. “
“The functionally generated path

(FGP) is a static representation of the opposing cusps’ dynamic eccentric movements from a centric position to achieve optimal articulation and occlusal harmony. When understood and appreciated, use of the FGP technique is a straightforward and practical method to achieve harmonious occlusal anatomy of restorations with the anterior determinant/anterior guidance, the posterior determinant/condylar guidance, existing occlusal and cuspal anatomy, and the neuromuscular system. Although the FGP technique is normally used in the fabrication of maxillary posterior indirect restorations, it is described and applied here in the fabrication of mandibular posterior restorations that maintained the patient’s bilateral group function many occlusion while eliminating the nonworking side and protrusive interferences. This novel procedure involved the use of a stone crib to intraorally construct a stone core that captured the FGP recording while simultaneously indexing to the contralateral and ipsilateral mandibular dentition. This technique lends additional stability to the stone core to minimize error during the mounting process. “
“This study analyzes the effects of loading a Kennedy class I implant-assisted removable partial denture (IARPD) using finite element analysis (FEA).

Vomiting

occurred in approximately 70% of migraineurs, of whom approximately one third vomited during the majority of migraine episodes. In those who experienced nausea, 30.5% indicated that it interfered with their ability to take their oral migraine medication. In those with vomiting, 42.2% indicated that it interfered with their ability to take their oral migraine medication. The treatment challenges posed by migraine-related nausea and vomiting selleck products remain unmet today, more than 15 years later, despite the availability of multiple triptans in several formulations. In a 2010 National Headache Foundation survey of 500 US migraineurs, 66% reported that nausea and/or vomiting accompany their migraines.[8] Among the patients who took prescription oral medication (n = 271), approximately 4 in 10 reported that they had delayed or avoided taking oral medication because of migraine-related nausea or vomiting. In April 2011, a round table of headache specialists and a gastroenterologist, funded by NuPathe Inc., was convened to explore unmet needs in the treatment of migraine vis-à-vis gastrointestinal signs and symptoms

and to assess strategies for helping to address those needs. This supplement summarizes the proceedings of that roundtable meeting. In his paper “Why Triptan Treatment Can Fail: Epigenetics Compound Library Focus on Gastrointestinal Manifestations of Migraine,” Dr. Larry Newman explores the contribution of gastrointestinal manifestations of migraine to triptan treatment failure.[9] He reviews clinic- and population-based data demonstrating that migraine-related nausea and vomiting and migraine-associated gastroparesis are prevalent and highly impactful. The oral therapies that dominate migraine treatment, he contends, do not satisfactorily address these gastrointestinal signs and symptoms. Oral triptans are not

the optimal therapy in the presence of migraine-related nausea because nausea predicts poor response to oral triptans and because nausea O-methylated flavonoid can cause patients to delay oral treatment, which can further compromise therapeutic efficacy. Moreover, oral triptans are not the optimal therapy in the presence of migraine-associated gastroparesis because these agents rely on gastric motility and gastrointestinal absorption and may be ineffective or slowly or inconsistently effective in the presence of gastroparesis. Dr. Mark Pierce extends this discussion by considering evidence relevant to the use of triptan tablets in the context of pretreatment and treatment-emergent nausea in his paper “Oral Triptans and Nausea: Treatment Considerations in Migraine.”[10] He reviews results from clinical trials databases showing that the presence of pretreatment nausea strongly predicts poor response to oral triptans. He also reviews data supporting the possibility that oral triptans contribute to development of nausea among patients with migraine and no nausea at pretreatment baseline.

22, 24 Next, Venetoclax through ChIP assays, we investigated the effect of miR-200a on the histone H3

acetylation level at its own promoter. Ectopic expression of miR-200a significantly increased the histone H3 acetylation level at the mir-200a promoter (Fig. 6C). We transfected pcDNA3.1-HDAC4 or pcDNA3.1 as the negative control into HepG2 cells, and 48 hours later, we examined acetyl-histone H3 by western blotting. The ectopic expression of HDAC4 significantly reduced global acetyl-histone H3 (Fig. 6D). Next, we transfected miR-200a mimics or the miRNA negative control into HepG2 cells, and 48 hours later, we examined global acetyl-histone H3 by western blotting. Our result demonstrated that miR-200a selleckchem up-regulated global acetyl-histone H3 (Fig. 6E). Recent studies have indicated that HDAC4 deacetylated histone H3 at the p21WAF/Cip1 promoter region.26, 29 Now that miR-200a could inhibit HDAC4 expression, we assessed, through ChIP assays, whether overexpression of miR-200a could increase histone H3 acetylation level at the p21WAF/Cip1 promoter. Our results indicate that ectopic expression of miR-200a significantly increases the histone H3 acetylation level at the p21WAF/Cip1 promoter (Fig. 6F). These results demonstrate that miR-200a induced aberrant histone acetylation in HCC by targeting HDAC4. To investigate the

biological effects of miR-200a on human HCC, we generated two stably transfected cell lines containing integrated click here copies of miR-200a or a control lentiviral expression vector. We observed significant up-regulation of miR-200a in the stably transfected cell lines compared with cells transfected with negative control (Fig. 7A). Overexpression of miR-200a inhibited cell proliferation (Fig. 7B) and migration (Fig. 7C,D) in vitro. The stably transfected cells were implanted subcutaneously into the flanks of nude mice. Up-regulation of miR-200a significantly decreased overall tumor growth, as assessed by measurements of tumor volume (Fig. 7E,F). The aberrant histone acetylation at the promoters of cellular genes is an important feature in the development of human cancers.30,

31 Many tumor suppressor genes, such as p21WAF/Cip1 and TMS1 (target of methylation-induced silencing 1), have been demonstrated to be silenced by promoter hypoacetylation.26, 32 The global inhibition of HDAC activity has been indicated to stimulate antitumor effects, and the approval of the HDAC inhibitor suberoylanilide hydroxamic acid by the US Food and Drug Administration for the treatment of cutaneous T cell lymphoma, validates the importance of histone acetylation in carcinogenesis.33, 34 However, the mechanism responsible for aberrations in histone acetylation remains largely unknown. In this study, for the first time, we identified miR-200a as both the target and the effector of aberrant histone acetylation in HCC.