These include the possibilities that markers might help to identify individuals at the risk of more rapid joint deterioration, that clotting factors may have additional local action within tissues, and that outcomes might be improved with therapies that directly address wound healing and inflammation. Joint assessment tools are important. Conventional radiography is frequently used, but given the possibility of subclinical joint bleeds, accurate non-invasive imaging tools are required to detect soft

tissue and cartilage changes. Magnetic selleck products resonance imaging and ultrasonography can prove valuable here. New imaging techniques should help to increase understanding of the biological basis of early events in haemophilic arthropathy. The optimal way to measure outcomes in haemophilia is to use several methods – in addition to imaging methods, a 360° approach will use physical, functional and quality-of-life instruments. In PWH, inhibitor development complicates treatment of joint bleeds and increases the risk of developing arthropathy. A new therapeutic approach for joint bleeds in inhibitor patients divides treatment into two phases: bleed control, with bypassing agent therapy until bleeding has definitely ceased, followed by regular dosing to prevent rebleeds until synovial recovery

is complete. “
“Summary.  While an estimated 13% of women with unexplained menorrhagia have von Willebrand disease (VWD), the frequency of

other potential bleeding disorders learn more has been uncertain. This study describes the relatively wide range of laboratory characteristics of women with unexplained menorrhagia and presents issues affecting diagnosis in this population. Women with pictorial blood assessment chart (PBAC) score >100 were identified at Amino acid six U.S. sites and asked to remain drug free for 10 days prior to testing. Blood was collected on one of the first four menstrual cycle days and tested at a central laboratory for procoagulant factors, VWD and fibrinolytic factors. Platelet function testing by PFA-100® (PFA) and platelet aggregation with ATP release (PAGG/ATPR) were performed locally using standardized methods. Among 232 subjects, a laboratory abnormality was found in 170 (73.3%), including 124 of 182 White (68.1%) and 34 of 37 Black (91.9%) subjects; 6.0% had VWD, 56.0% had abnormal PAGG/ATPR, 4.7% had a non-VWD coagulation defect (NVCD) and 6.5% had an abnormal PFA only. AGG/ATPR was reduced in 58.9% of subjects, with multiple agonists in 28.6%, a single agonist in 6.1% and ristocetin alone in 24.2%. Frequencies of PAGG/ATPR defects varied by study site and race; frequencies of VWD and NVCD were similar. Laboratory abnormalities of haemostasis, especially platelet function defects, were common among women with unexplained menorrhagia across multiple U.S. sites. To what degree these abnormalities are clinically significant requires further study.

Following in vivo APAP, LDK378 research buy a rapid decline in P-c-Src (not total Src) was observed in mitochondria but not cytoplasm. Knockdown of Sab with adeno-shSab prevented inactivation of mitochondrial c-Src after APAP in vivo. Next we found that DOK-4, Src binder (J Biol Chem. 280, 26383-96,2005), was expressed exclusively in mitochondria of hepatocytes. Liver mitochondria isolated after DOK-4 knockdown were resistant to direct P-JNK/ATP mediated inhibition of OCR. Knockdown of DOK-4 in vivo (adeno-shDOK-4) prevented de-phosphorylation

of active Src and markedly protected against APAP toxicity. Conclusions: The interaction of JNK with Sab leads to inactivation of intramitochondrial c-Src and impairment of respiration. The dephosphorylation of c-Src is dependent on DOK-4, a platform for binding of Src and Ptp. Knockdown of mitochondrial DOK-4 markedly protects against APAP hepatotoxicity. Therefore, dysregulation of intramitochon-drial c-Src kinase mediates the Sab dependent effects of JNK leading to impaired mitochondrial function in APAP toxicity. Disclosures: Neil Kaplowitz – Consulting: GlaxoSmithKline,

JNJ, Merck, Novartis, Hepregen, Takeda, Otsuka, Pfizer, Geron, Daiichi-Sanyo; Independent Contractor: Acetaminophen Litigation The following people have nothing to disclose: Sanda Win, Sorafenib mouse Tin A. Than Mechanisms of drug-induced liver injury (DILI) are incompletely understood. Hepatotoxicity from acetaminophen (APAP) poses widespread problems, including acute liver failure (ALF), and requires more therapeutic development. Although the Clostridium perfringens alpha toxin cell type-specific approach has typically been utilized for cytotoxic mechanisms, recent studies identified sharing of toxicity pathways and processes in a cell-agnostic manner. For instance, expression of N-methyl-D-aspartate receptors (NMDARs) is classically associated with excitoxic injury in neuronal tissues, e.g.,

ischemic or traumatic insults, Alzheimer’s, Parkinson’s, schizophrenia, etc., but rodent and human hepatocytes also expressed NMDAR activity after liver anoxia or injury. To determine whether NMDARs could contribute in APAP-induced hep-atotoxicity, we performed studies in cultured HuH-7 cells and primary mouse hepatocytes with or without NMDA and APAP, as well as NMDAR antgonists, MK801 or memantine. MTT assays were performed to assess cytotoxicity. Calcium fluxes were measured in hepatocytes with NMDA and NMDAR block-ers. Brain and liver tissues were examined for multiple NMDARs by RT-PCR, western, and immunostaining. C57BL/6 mice were used for studies with 500 mg/kg APAP with or without 30 mg/ kg memantine. Liver injury was evaluated by histology. We found HuH-7 cells and mouse hepatocytes expressed NMDARs and were sensitive to APAP-induced cytotoxicity, which was abolished by MK801 or memantine. In mouse hepatocytes, NMDA or quinolinic acid, another agonist of NMDAR, dose-de-pendently induced calcium fluxes, APAP alone did not directly stimulate calcium fluxes related to NMDARs.

The withdrawal time and experience level of the endoscopist were more important than the procedure order in detecting adenomas by colonoscopy. Key Word(s): 1. Time; 2. colon polyp; 3. adenoma; 4. procedure order Presenting Author: FUMIAKI KAWARA Additional Authors: TETSUYA YOSHIZAKI, YOSHIKO OHARA, SHINWA TANAKA, TSUKASA

ISHIDA, YOSHINORI MORITA, TAKASHI TOYONAGA, EIJI UMEGAKI, HIROSHI YOKOZAKI, TAKESHI AZUMA Corresponding Author: FUMIAKI KAWARA Affiliations: Kobe University Hospital, Kobe University Hospital, Kobe University Hospital, Kobe University Hospital, Kobe University Hospital, Kobe University PF-02341066 molecular weight Hospital, Kobe University Hospital, Kobe University Hospital, Kobe University Hospital Objective: Introduction: There remains many

unknown check details points about the diagnosis and the prognosis of duodenal polyps. In particular, little is known about the polyps which show gastric mucin phenotype by immunohistochemical staining. We report here the endoscopic and pathological findings of two duodenal polyp cases with gastric mucin phenotype. Methods: Case report: The patients were male in both cases, and the endoscopic examination revealed semipedunculated polyps over 20 mm in diameter in their duodenal bulb. Both polyps were soft and lobulated with reddish appearance, and some lobules had white deposition on them. In the Edoxaban case 1, microvascular dilation was observed at the top of the polyp by magnified narrow band imaging (NBI) system. On the other hand, the vasculature was uniform and regular without dilatation in case 2. Endoscopic mucosal resection (EMR) was performed for both cases. Pathological findings: The polyp in the case 1 was diagnosed as well differentiated tubular adenocarcinoma. It was hyperplastic polyp in the case 2. Evaluation by immunohistochemistry revealed that MUC5AC and MUC6 but not CD10 and MUC2 were expressed in both polyps, which confirmed the gastric mucin phenotype of these lesions.

Results: Discussion: Duodenal polyps with gastric mucin phenotype were thought to develop from the ectopic gastric mucosa, gastric metaplasia or Brunner’s gland. However, there are few reports about the characteristics of them, so the details are still unclear. Conclusion: We experienced both malignant and benign cases, which showed distinctive findings with NBI system. It would be important to accumulate the data of endoscopic features for the diagnosis of malignant or benign lobulated villous polyps with gastric mucin phenotype to analyze the correlation with pathological findings, which may also lead to the better understanding of the biological characteristics of these polyps. Key Word(s): 1. Duodenal polyp; 2. gastric mucin phenotype; 3.

This antisteatotic effect was probably the result of a combination of effects on key mechanisms driving the progression to hepatic steatosis,

especially those related to insulin resistance. In this regard, Alox15 deletion in ApoE−/− mice resulted in significant improvements in glucose and insulin tolerance tests in parallel with reduced JNK phosphorylation, an established marker of insulin resistance. Moreover, Alox15 disruption augmented phosphorylation of AMPK, a master regulator of glucose and lipid homeostasis, normalized the hepatic glycogen content, and up-regulated the expression of IRS-2. Given that we did not detect changes in fasting glucose, these findings are consistent with the notion that the effects on fasting glucose in ApoE−/− Alisertib order mice are modest, whereas effects on glucose tolerance and insulin tolerance are more pronounced.36 Additionally, the antisteatotic effect associated with Alox15 disruption in ApoE−/− Ivacaftor datasheet mice was related to insulin-sensitizing effects in adipose tissue. Indeed, the insulin-resistant adipokines MCP-1, TNFα, IL-6, and resistin

were significantly repressed, whereas the expression of GLUT-4 was induced in ApoE−/−/12/15-LO−/− mice. Overall, the genetic disruption of Alox15 rendered similar effects on hepatic insulin signaling to those reported in previous studies in muscle and adipose tissues and are consistent with the role of 12/15-LO as a positive modulator of the onset of insulin resistance.9, 10, 13-16 It is important to note that the antisteatotic effects accompanying Alox15 disruption in ApoE−/− mice occurred in the absence of changes in liver weight, a phenomenon that has been documented.27, 37 The mechanisms by which hepatic steatosis does not translate into increased liver weight in ApoE−/− mice are presently unknown, but it can be speculated that the ApoE protein, in addition to its role

in lipoprotein clearance and very low-density lipoprotein assembly–secretion, also modulates the chemical composition of the hepatic tissue. Moreover, disruption of Alox15 in ApoE−/− mice did not affect serum cholesterol elevations, over suggesting that amelioration of liver injury in this model is independent of serum cholesterol levels. Although this is an intriguing observation, it is in line with previous publications in which deletion of Alox15 in ApoE−/− mice did not induce changes in serum cholesterol levels.11, 12, 38 Finally, it is also important to recognize that the antisteatotic effects accompanying the disruption of Alox15 in ApoE−/− mice differ slightly from those observed after disruption of Alox5 in these mice.7 In particular, disruption of the Alox5 gene significantly reduced hepatic inflammation without modifying the degree of hepatic steatosis,7 whereas the current study demonstrates that disruption of the Alox15 gene markedly reduces both parameters of liver injury. These results suggest that in terms of NAFLD, 12/15-LO appears to be the most relevant LO pathway.

We therefore conducted a large, pooled, post hoc analysis of patients with HCV genotypes 1, 4, 5, or 6 from four trials of PEG-IFN alfa-2a and ribavirin therapy to better understand the association between KU-57788 datasheet virologic response and pharmacodynamic effects as reflected by changes in hematologic parameters and body weight. HCV, hepatitis C virus; IFN, interferon; PEG-IFN, pegylated interferon; SVR, sustained virologic response. Patients with HCV genotypes 1, 4, 5, or 6 receiving 24 or 48 weeks of combination therapy with PEG-IFN alfa-2a (Pegasys; Roche, Nutley, NJ; 180 μg/week) and ribavirin (Copegus; Roche, Nutley, NJ; 1,000 or 1,200 mg/day) were pooled from

two registration trials1, 2 and two phase 4 trials.7, 8 The registration trials were randomized, multicenter, phase 3 studies in IFN-naïve patients with chronic hepatitis C; the first trial compared the efficacy of PEG-IFN alfa-2a and ribavirin therapy with IFN alfa-2b and ribavirin therapy for 48 weeks,1 and the second trial of PEG-IFN alfa-2a and ribavirin JNK inhibitor nmr therapy compared different treatment duration and ribavirin dose combinations.2 The phase 4 studies were noncomparative, open-label studies of PEG-IFN alfa-2a

and ribavirin for 48 weeks in treatment-naïve patients with HCV genotype 1; the majority (>73%) of patients in the first study were African American patients,7 and the second study was conducted in Latino and non-Latino Caucasian patients (ClinicalTrials.gov Identifier NCT00087607).8 All studies included stopping rules for nonresponse except for the trial in African American patients.7 Patients

who received PEG-IFN monotherapy Tyrosine-protein kinase BLK or IFN alfa-2b and ribavirin combination therapy (Rebetron) and patients with HCV/human immunodeficiency coinfection were excluded from the study. The objectives of this study were: (1) to explore the association between pharmacodynamic parameters and virologic response category (SVR, relapse, breakthrough, and nonresponders); (2) to explore the association between pharmacodynamic parameters and race/ethnicity (African American, Latino Caucasians, non-Latino Caucasians, and other races); and (3) to evaluate the effects of clinically significant hemoglobin decline (>3 g/dL versus ≤3 g/dL) on SVR. The pharmacodynamic effects of interest in this analysis were hematologic parameters (hemoglobin level, neutrophil count, and platelet count) and weight loss. Maximum decrease (baseline value for the hematologic test minus the lowest value for that test while on therapy) was used to assess the change in hematologic parameters. To better adjust for the impact of baseline difference, percentage of change from baseline was used to analyze racial/ethnic group differences and body weight changes. For patients without the specified hematologic test or body weight measurement during treatment, the corresponding maximum decrease was set as missing.

Conclusion: Hepatocyte-derived type III IFNs contribute to ISG induction and antiviral activity, but are not the principal determinant of the outcome of HCV infection. (HEPATOLOGY 2012;56:2060–2070) HCV poses a significant health problem, with more than 170 million chronically infected people worldwide.1 Treatment is based on interferon (IFN)-α in combination with ribavirin and direct antiviral agents,2 but

the role of IFN-α and other IFNs in the spontaneous outcome of infection is unclear. Type I IFNs (13 IFN-α proteins plus IFN-β, IFN-ε, IFN-κ, and IFN-ϖ) form the frontline of innate host defenses by inducing an antiviral state in infected and neighboring cells, and by modulating adaptive immune responses directly and by the induction of IFN-stimulated genes ISGs.3 Whereas ISGs are strongly induced during HCV infection,4, 5 neither the ISG-inducing cytokines nor their Roxadustat price cellular Palbociclib sources have been defined. HCV has been shown to interfere with Toll-like receptor (TLR)3- and retinoic-acid–inducible gene (RIG) I–mediated induction of IFN-β and with Janus kinase/signal transducer and activator of transcription (JAK-STAT) signaling downstream of the IFN-α/β receptor,6 thus reducing IFN-α/β production to levels that are undetectable in HCV-infected patients. In vitro studies suggest that plasmacytoid dendritic cells (pDCs) may be the source of the ISG-inducing type I IFNs,7

but the role of pDCs has not been studied in the HCV-infected liver. In this context, type III IFNs have Y-27632 2HCl become of interest. This family is composed of interleuking (IL)-29, IL-28A, and IL-28B, and induced in response to several viral pathogens.8 Although signaling by the JAK-STAT pathway is shared with type I IFNs and similar sets of ISGs are induced,9 receptors for type III IFNs are distinct from those for type I IFNs10 and are expressed in a cell-type–specific manner.11 In the liver, type III IFN receptors are expressed at significant levels as a functional full-length form,10, 11 suggesting intact type III IFN signaling as part of the intrahepatic innate immune response.

Furthermore, single nucleotide polymorphisms (SNPs) near and within IL28B are strong predictive markers for spontaneous, treatment-induced HCV clearance,12-15 suggesting that variations in type III IFN expression or function affect the outcome of HCV infection. In this context, Langhans et al. reported that IL-29 serum levels do not differ between patients with acute HCV infection and healthy controls, but that they are lower in chronically infected patients.16 Whereas recombinant type III IFNs are known to suppress HCV replication in vitro,17-19 their expression level in the liver has never been studied prospectively during acute HCV infection. Thus, the relative antiviral effect of endogenously produced type I and type III IFNs is not known.

5A]). Hepatic expression of SREBP-1c, ACC1, and FAS was higher in IL-6−/− mice but lower in IL-10−/− mice compared with those in

WT mice (Fig. 5A,B). Reduced expression of these genes in IL-10−/− mice was partially reversed in IL-10−/−IL-6−/− dKO mice (Fig. 5A,B). Activation of adenosine monophosphate-activated protein kinase (AMPK) plays a key role in controlling lipid metabolism by phosphorylating and subsequently inhibiting ACC and suppressing the expression of ACC and FAS through down-regulation of SREBP-1c.32 ACC is an important enzyme for fatty acid synthesis, which catalyzes the first step in de novo fatty acid biosynthesis by converting acetyl coenzyme A to malonyl coenzyme A. Malonyl coenzyme A acts as a potent inhibitor of fatty acid oxidation by inhibiting carnitine palmitoyltransferase 1 (CPT-1), BMN-673 which transports fatty acids into the mitochondria for oxidation.33, 34 As shown in Fig. 5, expression of activated (i.e., phosphorylated) AMPK (pAMPK) was significantly higher in IL-10−/− mice than that in WT mice in both the XL184 price STD and

HFD groups, whereas such up-regulation was diminished in IL-10−/−IL-6−/− mice. Expression of pAMPK was comparable between IL-6−/− mice and WT mice. Consistent with the elevated levels of pAMPK, IL-10−/− mice had higher levels of inhibited (i.e., phosphorylated) ACC1 (pACC1) compared with WT mice. Such elevated phosphorylated ACC1 was reduced in IL-10−/−IL-6−/− mice versus IL-10−/− mice. In addition, hepatic expression of CPT1 was higher in HFD-fed IL-10−/− mice compared with WT mice. An additional deletion of IL-6 reduced hepatic CPT1 expression in IL-10−/−IL-6−/− mice versus IL-10−/− mice. Expression of these lipid metabolism-associated genes were also examined in WT, IL-10−/−, and IL-10−/− STAT3Hep−/− mice (Fig. 6). Compared with WT mice, IL-10−/− mice had reduced expression of SREBP-1c, ACC1, and Exoribonuclease FAS but enhanced expression of pAMPK, pACC1, and CPT-1 in the liver. These

dysregulations were partially corrected in IL-10−/− STAT3Hep−/− mice. In this article, we have demonstrated that IL-10−/− mice have greater liver inflammatory response but less steatosis and liver injury compared with WT mice after feeding with an ETOH or HFD diet. Our data suggest that in our models, inflammatory response reduces rather than promotes steatosis through activation of hepatic IL-6/STAT3, which subsequently inhibits the expression of lipogenic genes (SREBP-1c, ACC1, and FAS). In concert, IL-6 up-regulates the expression of CPT-1 and activates AMPK, which in turn further attenuates the expression of SREBP-1c and its target genes and inhibits ACC1. We have integrated our findings in a model depicting the effects of inflammation on steatosis in IL-10−/− mice (Fig. 7).

In contrast, rifaximin has not been shown to have a significant side-effect profile,16 certainly when compared to other previously utilized antibiotics, although long-term data are not yet available. Some of the adverse effects of lactulose can be minimized with the use of lactitol (an analog of lactulose);17 however, this is not available worldwide. Overtreatment of lactulose can lead to the more serious side-effects of marked dehydration, hyponatremia, and worsening of hepatic encephalopathy.5 The dosing regime of rifaximin can check details be either fixed daily or cyclical,15 whereas lactulose does rely on some degree of patient adjustment to ensure approximately two to three semiformed

stools daily. Costing considerations are

not straightforward. While the direct cost of rifaximin compared to lactulose is marked, approximately $US1120 as opposed to $150 per month in the USA,15 the total annual costing of rifaximin has been reported to be less than lactulose when hospital admissions are taken into account.18 The role of rifaximin in the prevention or treatment of hepatic encephalopathy following an acute variceal bleed remains to be elucidated. Even if no further conclusive studies confirming the beneficial effect of lactulose occur, it is difficult to conceive of it being substituted as first-line therapy for hepatic encephalopathy. Its routine prophylactic use in the setting of an acute variceal bleed LY2157299 (post-initial stabilization and endoscopic

control of bleeding) seems intuitive. Perhaps prophylactic lactulose therapy should be considered for incorporation into acute variceal bleed practice guidelines as the “standard of care. “
“Hereditary hemochromatosis (HH) is an autosomal recessive disease caused by mutations in the HFE gene leading to increased iron absorption and deposition of iron in various organs, including the liver. It is the most common hereditary disorder in White people with a prevalence as high as one in 140 although phenotypic expression is much less common. It typically presents as asymptomatic elevation in iron studies IMP dehydrogenase but can present with abnormal liver enzymes and hepatomegaly. Arthralgias, loss of libido, diabetes and heart failure can occur due to iron deposition in other organs. The diagnosis relies on demonstration of a high iron saturation and ferritin. Testing for HFE gene mutations and liver biopsy can also be helpful. Treatment is based on depletion of iron through phlebotomy and improves survival. “
“A woman, aged 76, was admitted to hospital with abdominal pain that had persisted for 24 hours. On examination, she had a smooth mass in the right upper quadrant of her abdomen. Seventeen years previously, she had been diagnosed with two hepatic cysts; one had been treated by percutaneous sclerotherapy while the other had been left untreated.

Algae are critical parts of aquatic ecosystems that power food webs and biogeochemical cycling. Algae are also major sources of problems that threaten

many ecosystems goods and services when abundances of nuisance and toxic taxa are high. Thus, algae can be used to indicate ecosystem goods and services, which complements how algal indicators are also used to assess levels of contaminants and Selleck C59 wnt habitat alterations (stressors). Understanding environmental managers’ use of algal ecology, taxonomy, and physiology can guide our research and improve its application. Environmental assessments involve characterizing ecological condition and diagnosing causes and threats to ecosystems goods and services. Recent advances in characterizing condition include site-specific models that account for natural variability among habitats to better

estimate effects of humans. Relationships between algal assemblages and stressors caused by humans help diagnose stressors and establish targets for protection and restoration. Many algal responses to stressors have thresholds that are particularly important for developing stakeholder consensus for stressor management targets. Future research on the regional-scale resilience of algal assemblages, the ecosystem goods and services they provide, and methods for monitoring and forecasting change will improve water resource management. “
“Until the recent use of molecular markers, species Vincristine in vitro diversity of Lobophora, an ecologically important brown algal genus with a worldwide distribution in temperate and tropical seas, has been critically underestimated. Using a

DNA-based taxonomic approach, we re-examined diversity of the genus from New Caledonia in the Southwest Pacific Ocean. First, species were delineated using general mixed Yule coalescent-based and barcoding gap approaches applied to a mitochondrial cox3 data set. Flavopiridol (Alvocidib) Results were subsequently confirmed using chloroplast psbA and rbcL data sets. Species delimitation analyses agreed well across markers and delimitation algorithms, with the barcoding gap approach being slightly more conservative. Analyses of the cox3 data set resulted in 31–39 molecular operational taxonomic units (MOTUs), four of which are previously described species (L. asiatica, L. crassa, L. nigrescens s.l., L. pachyventera). Of the remaining MOTUs for which we obtained a representative number of sequences and results are corroborated across analyses and genes, we described 10 species de novo: L. abaculusa, L. abscondita, L. densa, L. dimorpha, L. gibbera, L. hederacea, L. monticola, L. petila, L. rosacea, and L. undulata. Our study presents an excellent case of how a traditional morphology-based taxonomy fails to provide accurate estimates of algal diversity.

Although it is conceivable that Latino individuals may have less risk for fibrosis as an ethnic group, it is likely that the lower frequency of advanced Cilomilast research buy fibrosis may be explained, at least in part, by the overall younger age of the Latino population in this study. A notable finding of this study is the differential effect of HOMA-IR on risk of NASH (versus non-NASH histology), such that HOMA-IR conferred an increased risk of NASH in non-Latino whites, but not in Latinos. We did not find a differential effect of HOMA-IR on the risk of advanced fibrosis. Several studies

have described racial and ethnic variations in NAFLD, primarily with respect to differences in frequency of the disorder, with consistent reporting

of increased frequency in Latino populations and decreased frequency among African Americans. 3, 4, 7, 8, 23 Although the NASH CRN was not designed to be a population-based study, within our group of study participants with NAFLD, we found an increased frequency of NASH histology among Latinos (63%), compared to non-Latino blacks (52%), which LDE225 in vitro is in keeping with previously published trends. Although many studies of racial and ethnic variation in NAFLD have focused primarily on the prevalence (or frequency) of the disorder, a few studies have delved further into metabolic associations of NAFLD in different

racial and ethnic groups. A recently published study by Lomonaco et al. compared Hispanic and Caucasian individuals with biopsy-proven NASH with respect to several metabolic features, including measures of adipose and hepatic insulin resistance. The investigators found no significant difference between Hispanic and Caucasian individuals with respect to NASH severity, but their data suggested that in Hispanic diabetic patients, there may be a trend toward increased risk for fibrosis progression, warranting further investigation. 24 In two separate Cyclooxygenase (COX) investigations from the population-based Dallas Heart Study, Browning et al. and Guerrero et al. investigated the well-described dissociation between NAFLD and stereotypical metabolic risk factors, such as insulin resistance and obesity, among different racial and ethnic groups. 3, 9 Using magnetic resonance spectroscopy (MRS) to detect hepatic steatosis in a multiethnic population-based sample, Browning et al. reported the highest prevalence of hepatic steatosis among Latinos (45%) and lowest prevalence of steatosis among African Americans (24%), with whites having an intermediate prevalence of 33%. They also speculated that the increased prevalence of hepatic steatosis among Latinos might be attributable to the high prevalence of obesity and insulin resistance in this ethnic group.