26 Remarkably,

26 Remarkably, Selleck Belnacasan when HCC patients were classified

into low- and high-survival groups on the basis of global gene expression profiling of their liver samples,27 high Gal-1 expression was associated with low survival. Thus, in inflammation-mediated hepatocarcinogenesis, Gal-1 may act as a protective anti-inflammatory agent during early stages of chronic liver pathology but as a protumorigenic agent during the late stages of the disease. On the basis of our finding that endogenous Gal-1 protects the liver against ConA-induced hepatitis in the B6 strain but not in the FVB strain (Fig. 7), we hypothesize that the increased inflammation (and aberrant regulation of multiple immune/inflammatory genes) in the Mdr2-KO/FVB strain can be explained in part by the impaired anti-inflammatory activity of Gal-1. This hypothesis is supported by the up-regulation of other anti-inflammatory genes (e.g., Slpi) specifically in the Mdr2-KO/FVB strain (Supporting Table 2), more robust Gal-1 induction in the Mdr2-KO/B6 liver versus the Mdr2-KO/FVB liver at the age of 1 month (Fig. 6C,D), and the induction of proinflammatory Tamoxifen Tnfa, Il2, and Cxcl2 as well as anti-inflammatory Slpi after ConA challenge in Gal-1–KO/B6 mice (Fig. 7E,F). Several genes that were differentially expressed only in the Mdr2-KO/B6 strain are involved in the regulation of NF-κB signaling: trefoil factor 3 (Tff3)

and TRAF-interacting protein with forkhead-associated domain (Tifa), which were up-regulated, and hexamethylene bisacetamide inducible 1 (Hexim1), which was down-regulated (Supporting Table 2). Tff3 may transiently activate NF-κB,28 and Tifa also activates NF-κB,29 whereas Hexim1 inhibits NF-κB–mediated transcription.30 These examples indicate differential regulation of the NF-κB signaling pathway between the two Mdr2-KO

strains. Among genes up-regulated in the Mdr2-KO/FVB mice but down-regulated in the Mdr2-KO/B6 mice (Supporting Table 2), Angptl4, Lpin1, and Lpin2 encode regulators of lipid metabolism, and Por encodes cytochrome P450 reductase. In line with reduced chronic inflammation in Mdr2-KO/B6 mice, many genes involved in response to oxidative stress were up-regulated in the Mdr2-KO/FVB MCE公司 strain but not in the Mdr2-KO/B6 strain. This effect of the Mdr2-KO/B6 liver could be caused in part by down-regulation of the Por and Lipin-1 proteins. Por may be a source of endogenous oxidative DNA damage and genetic instability,31 and Lipin-1 promotes fatty acid oxidation.12 Importantly, the gene Aif1, encoding Aif1, was up-regulated in the Mdr2-KO/FVB liver4 but not in the Mdr2-KO/B6 liver (Fig. 4C). Aif1 is a crucial mediator in the inflammatory response, which may enhance NF-κB transcriptional activity and facilitate tumor growth,32 and thus serves as a central node in coexpression networks connecting obesity-associated genes in the liver and other tissues.

This study involved unrelated HCC and LC patients of Korean ethni

This study involved unrelated HCC and LC patients of Korean ethnicity treated at the Asan Medical Center, Seoul, Korea. Disease diagnosis was confirmed by histopathology. Previous clinical history, enzyme-linked immunosorbent assay (ELISA)-based serum test results for hepatitis B virus (HBV) and hepatitis C virus (HCV), and clinical laboratory data were collected for these individuals; 89% of the HCC cases and 76% of the LC cases were chronically infected with either HBV or HCV. Two sources of controls were used. The first set of controls for our study was unrelated individuals from

the Asan Medical Palbociclib nmr Center. The viral infection status of controls was not ascertained. A second set of controls was HBV+ individuals of Chinese origin (described previously).6 The local ethics committees and all subjects gave informed consent before inclusion in the study. A total of 386 Korean HCC cases, 86 Korean LC cases, 587 Korean controls (Supporting Table S1), and 100 Chinese controls passed the quality control evaluations (DNA integrity measurement, STRP genotyping for assessment of identity, and high SNP call rate from the Affymetrix 6.0 platform) described below. We confirmed through molecular assays that there is no population stratification among the Korean samples (see Supporting Methods). Individuals from the Korean population set were assigned to the discovery

(Stage 1) or validation selleckchem (Stage 2) group based on their order of enrollment in

the study. Stage 1 included 271 上海皓元 controls, 180 HCC cases, and 66 LC cases; Stage 2 had 316 controls, 206 HCC patients, and 20 individuals with LC. Key findings from the two-stage analysis were further validated using the Chinese control samples. Peripheral blood DNA was extracted using the Blood DNA Kit (Qiagen, Valencia, CA). DNA integrity and quantity were assessed using the Quantifiler Human DNA Quantification kit (Applied Biosystems, Foster City, CA). Polymerase chain reaction (PCR) products were analyzed with an ABI 3130XL Automated DNA Sequencer and the GeneMapper ID v3.2 software (Applied Biosystems, Foster City, CA). The Affymetrix SNP6.0 assay was performed according to the manufacturer’s instructions (Affymetrix, Santa Clara, CA). Assay runs were performed in 96-well plates containing equal numbers of case and control samples, two Asian HapMap samples (chosen from NA18954, NA18971, NA18603, and NA18995) for external genotype validation, the Affymetrix Affy103 control DNA, and a water blank. Cases were randomly selected for each plate one-by-one using a random-number generator. Each case in the discovery phase was paired with its best match in sex and age among the control samples. Processing each Stage 1 case along with a matched control was aimed at minimizing technical variation in experimental results.

We then discuss its relative importance in comparison with altern

We then discuss its relative importance in comparison with alternative mechanisms that could be maintaining genetic and phenotypic diversity. The idea that the fitness of an organism is affected by the relative frequencies of the genotypes in

a population was first described by Fisher (1930), suggesting that an inverse relation between the two could maintain stable polymorphisms. This concept was later formalized by other researchers, such as Li (1955), Wright (1956) and Lewontin (1958), who developed mathematical models to describe the mechanism. Evidence that the fitness of a morph depends on its frequency relative to the frequencies of the other morphs was first found by Wright & Dobzhansky (1946) in an experimental Doxorubicin molecular weight population of Drosophila pseudoobscura. PF-02341066 research buy Three different gene arrangements can be found in the third chromosome of this species, and their frequencies were observed to fluctuate over the year in natural populations. Wright and Dobzhansky set up an experimental population with known frequencies of the different genotypes and controlled environmental conditions. They found that the observed changes in frequencies of the phenotypes at different temperatures fitted the predictions of a model where the fitness of the homozygotes decreases

as their frequencies increase, while the fitness of the heterozygotes remains constant. However, Wright and Dobzhansky considered this hypothesis to be an ‘extreme’ one. Since then, there have been several laboratory studies where evidence for NFDS has been found in populations of Drosophila, with morph frequencies fluctuating MCE in a manner that is predictable based on the known effects of frequency on

fitness (Levene, Pavlovsky & Dobzhansky, 1954; Kojima & Tobari, 1969; Anderson & Brown, 1984; Singh & Chatterjee, 1989). A correlation between fitness and frequency has also been found in laboratory studies in crustaceans (Maskell et al., 1977; Duncan & Little, 2007), land snails (Tucker, 1991) and water snails (Koskella & Lively, 2009). This correlation has been found in natural populations as well, and is the commonest form of evidence supporting NFDS in the wild (Reid, 1987; Gross, 1991; Seehausen & Schluter, 2004; Svensson et al., 2005; Olendorf et al., 2006; Bleay et al., 2007; Takahashi & Watanabe, 2010). A few studies have also demonstrated oscillations in morph frequencies over time that can be explained by NFDS (Hori, 1993; Sinervo & Lively, 1996). However, direct evidence for NFDS in the wild is generally scarce because the best way to test for it is to manipulate the frequencies of different morphs in a population, and to obtain reliable measures of fitness from individuals of each morph, both of which pose considerable practical challenges.

However, some clinical concerning issues

However, some clinical concerning issues ABT-199 mw have not been investigated. Methods: we explored the pharmacokinetics and therapeutic efficacy of GX1-rmhTNFα by means of multimodality imaging(SPECT,Bioluminescence imaging, Contrast enhanced ultrasound).TUNEL assay and Immunohistochemistry staining were applied to assess the therapeutic efficacy. Histopathologic examination and biochemistry analysis were also used to assess its side-effects Results: SPECT and biodistribution study revealed specific accumulation of GX1-rmhTNFα in tumors (0.66±0.04%ID/g, 22 times vs. muscle 24h p. i.). BLI, in addition, showed satisfied growth delayed of luciferase expressing

tumors (SGC7901-Fluc) treated with GX1-rmhTNFα in comparison with 0.9 % saline (P<0.001). Postmortem tumor weight also showed a similar tendency (P<0.001). CEUS and CD31 staining demonstrated GX1-rmhTNFα could reduce blood perfusion and induce vascular degradation. TUNEL assay and Ki67 staining indicated pro-apoptosis and anti-proliferation property of GX1-rmhTNFα. Moreover, histopathologic examination and biochemistry analysis indicated limited specific renal or hepatic toxicity of GX1-rmhTNFα. Conclusion: In conclusion, this NVP-LDE225 study demonstrated that GX1-rmhTNFα was a safe and potent anticancer agent, which may have great potential for target therapy of gastric cancer. Key Word(s): 1. Targeted

therapy; 2. Fusion toxin; 3. Gastric cancer; 4. Molecular imaging; Presenting Author: SHUHUI LIANG Additional Authors: XIAOLI HUI, JIAN XU, YANXIANG LV, JING ZHANG, HAO HU, YONGZHAN NIE, BIAOLUO WANG, KAICHUN WU, JIE

DING, DAIMING FAN Corresponding Author: BIAOLUO WANG, KAICHUN WU, JIE DING Affiliations: Xijing Hospital of Digestive Diseases & State Key Laboratory of Cancer Biology; First Affiliate Hospital medchemexpress of Xi’an Jiao Tong University Objective: The vascular-endothelial-cell-specific binding peptide in gastric cancer GEBP11 (CTKNSYLMC) may be a potential candidate for targeted drug delivery in antivascular therapy and diagnosis of gastric cancer. The aim of this study is to further identify the ability of GEBP11 to target the vasculature of gastric cancer in vivo and evaluate the applicability of GEBP11 in neovasculature imaging diagnosis and antiangiogenesis therapy of gastric cancer. Methods: Immunochemical or immunofluorescent staining was performed to identify the subcellular location and the tumor vascular binding specificity of GEBP11. Receptor binding assay was performed to analyze quantitatively the binding specificity and affinity of GEBP11 to ECs. Binding assays in vivo, biodistribution assay and SPECT imaging were used to identify the targeting ability of GEBP11 to tumor tissues in vivo.. BLI or CLI imaging was used for monitoring and evaluation of therapeutic effect in internal radiotherapy experiment.


“The purpose was to assess the cost-effectiveness of soraf


“The purpose was to assess the cost-effectiveness of sorafenib in the treatment of hepatocellular carcinoma (HCC) patients GSK2126458 incorporating current prices and the results of the recent published field practice SOraFenib Italian Assessment (SOFIA) study. We created a Markov Decision Model to evaluate, in a hypothetical cohort of Caucasian male patients, aged 67 years with Barcelona Clinic Liver Cancer (BCLC) C HCC, or

BCLC B HCC who were unfit or failed to respond to locoregional therapies, well compensated cirrhosis, and with performance status 0-1 according to Eastern Cooperative Oncology Group (ECOG), the cost-effectiveness of the following strategies:

(1) full or dose-adjusted sorafenib for BCLC B and C patients together; (2) full or dose-adjusted sorafenib for BCLC B patients; (3) full or dose-adjusted sorafenib for BCLC C LY2606368 chemical structure patients. Outcomes include quality-adjusted life years (QALYs), costs, and incremental cost-effectiveness ratio (ICER). In the base-case analysis dose-adjusted sorafenib was the most effective of the evaluated strategies. For dose-adjusted sorafenib, QALY was 0.44 for BCLC B and C patients together, 0.44 for BCLC C patients, and 0.38 for BCLC B patients. The ICER of dose-adjusted sorafenib compared with BSC was €34,534 per QALY gained for BCLC B and C patients together, €27,916 per QALY gained for BCLC C patients, and €54,881 per QALY gained for BCLC B patients. Results were sensitive to BSC survival rate, and sorafenib treatment duration. Conclusion: In daily practice dose-adjusted, but not full-dose, sorafenib is a cost-effective treatment compared to BSC in intermediate and advanced HCC. (HEPATOLOGY 2013) Hepatocellular carcinoma (HCC) is the fifth most common cancer worldwide with more than half a million new cases each year with an increasing incidence in the USA and Europe, and contributes substantially

to healthcare spending. Most patients with HCC (∼50%) diagnosed at the Barcelona Clinic Liver Cancer (BCLC) are B (intermediate) and C (advanced) stages. The prognosis is grim for advanced HCC or intermediate 上海皓元 HCC patients who are contraindicated for or do not respond to locoablative treatments like transarterial chemoembolization (TACE) or radiofrequency ablation (RFA). 1-3 Sorafenib (Nexavar, Bayer Healthcare Pharmaceuticals-Onyx Pharmaceuticals) is an oral multikinase inhibitor that restrains tumor blood vessel development and tumor cell proliferation. Clinical efficacy data came from the Sorafenib Hepatocellular Carcinoma Assessment Randomized Protocol (SHARP) study, which was a registration multicenter, double-blind, placebo-controlled randomized trial in patients with advanced HCC.


“The purpose was to assess the cost-effectiveness of soraf


“The purpose was to assess the cost-effectiveness of sorafenib in the treatment of hepatocellular carcinoma (HCC) patients CH5424802 in vitro incorporating current prices and the results of the recent published field practice SOraFenib Italian Assessment (SOFIA) study. We created a Markov Decision Model to evaluate, in a hypothetical cohort of Caucasian male patients, aged 67 years with Barcelona Clinic Liver Cancer (BCLC) C HCC, or

BCLC B HCC who were unfit or failed to respond to locoregional therapies, well compensated cirrhosis, and with performance status 0-1 according to Eastern Cooperative Oncology Group (ECOG), the cost-effectiveness of the following strategies:

(1) full or dose-adjusted sorafenib for BCLC B and C patients together; (2) full or dose-adjusted sorafenib for BCLC B patients; (3) full or dose-adjusted sorafenib for BCLC C Adriamycin mw patients. Outcomes include quality-adjusted life years (QALYs), costs, and incremental cost-effectiveness ratio (ICER). In the base-case analysis dose-adjusted sorafenib was the most effective of the evaluated strategies. For dose-adjusted sorafenib, QALY was 0.44 for BCLC B and C patients together, 0.44 for BCLC C patients, and 0.38 for BCLC B patients. The ICER of dose-adjusted sorafenib compared with BSC was €34,534 per QALY gained for BCLC B and C patients together, €27,916 per QALY gained for BCLC C patients, and €54,881 per QALY gained for BCLC B patients. Results were sensitive to BSC survival rate, and sorafenib treatment duration. Conclusion: In daily practice dose-adjusted, but not full-dose, sorafenib is a cost-effective treatment compared to BSC in intermediate and advanced HCC. (HEPATOLOGY 2013) Hepatocellular carcinoma (HCC) is the fifth most common cancer worldwide with more than half a million new cases each year with an increasing incidence in the USA and Europe, and contributes substantially

to healthcare spending. Most patients with HCC (∼50%) diagnosed at the Barcelona Clinic Liver Cancer (BCLC) are B (intermediate) and C (advanced) stages. The prognosis is grim for advanced HCC or intermediate medchemexpress HCC patients who are contraindicated for or do not respond to locoablative treatments like transarterial chemoembolization (TACE) or radiofrequency ablation (RFA). 1-3 Sorafenib (Nexavar, Bayer Healthcare Pharmaceuticals-Onyx Pharmaceuticals) is an oral multikinase inhibitor that restrains tumor blood vessel development and tumor cell proliferation. Clinical efficacy data came from the Sorafenib Hepatocellular Carcinoma Assessment Randomized Protocol (SHARP) study, which was a registration multicenter, double-blind, placebo-controlled randomized trial in patients with advanced HCC.

Methods: Twenty

refractory FD patients with high levels o

Methods: Twenty

refractory FD patients with high levels of emotional distress who have failed to all motility-type agents or other gastrointestinal treatments were as FD group. Twenty healthy people were chosen as control. Personality traits and VT were observed for every people. Eysenck Personality MLN2238 Questionnaire (EPQ) was used to assess the personality of neuroticism (N), psychoticism (P), extroversion (E), phlegmatic temperament, sanguine temperament, choleric temperament and melancholic temperament. HF and RMSSD as the indices of HRV were measured by 24 h Holter, which were used to as the indicator of vagal tone (VT). The low VT was low HF and RMSSD declining. Results: (1) The value of HF and RMSSD were significantly lower in FD group than healthy group (P < 0.05); (2) The scores of P and N in FD group were higher check details than those of healthy group (P < 0.05);

But the scores of E in FD group was lower (P < 0.05); (3) The declining HF was related to neuroticism (N) in two groups (P < 0.05), which was no relationship with psychoticism (P) and extroversion (E) (P > 0.05); Interestingly, the patients with melancholic temperament have lower HF than other traits in healthy group (p < 0.05). Conclusion: The study found that the refractory FD patients have personality tendency of neuroticism, introversion, psychoticism, and low VT. In the healthy group, the personality of melancholic temperament (low scores of E and high scores of N) also has appeared low HF, and low HF was related to high N. These results show melancholic 上海皓元 temperament has tendency of vagus nerve dysfunction, and this trait may be more easily to suffer from refractory FD. Therefore, refractory FD may be based on personality traits, especially melancholic temperament. Key Word(s): 1.

Refractory FD; 2. Personality Traits; 3. Vagal Tone; Presenting Author: XINGYU LIU Additional Authors: HAO LIANG Corresponding Author: XINGYU LIU Affiliations: Chinese PLA General Hospital; Chinese PLA General Hospital Objective: To analyze the clinical and endoscopic characteristics, and treatment methods of 11 adult Henoch-Schonlein Purpura (HSP) with gastrointestinal involvement so as to improve the early diagnosis and treatment of this disorder. Methods: A retrospective study in 11 adult HSP patients with gastrointestinal involvement enrolled from 2008 to 2012 at Chinese PLA General Hospital was conducted. Results: The 11 adult HSP patients with gastrointestinal involvement enrolled in this study were mainly youth, and 5 patients (45.4%) have obvious inducing causes. All the patients had cutaneous purpura and abdominal pain, and the severity of abdominal pain was not concordant with physical signs. Abdominal pain occurred prior to cutaneous purpura in 7 patients (63.6%), and 8 patients (72.7%) had gastrointestinal bleeding.

The Rodin trial has extended our thoughts on this issue because i

The Rodin trial has extended our thoughts on this issue because it is a robustly populated

prospective observational study, in contrast to previously published results, which have been generated from smaller, retrospective, mostly uncontrolled heterogeneous population studies. Based on the results of 574 previously untreated severe haemophilia A patients (FVIII Paclitaxel ic50 activity, <0.01 IU mL−1), the observations in Rodin indicated that there was no difference in the incidence of alloantibody inhibitors whether patients received plasma-derived or recombinant full-length FVIII products (adjusted hazards ratio = 0.96). Furthermore, among those who developed alloantibody inhibitors while on plasma-derived FVIII concentrates, the content of von Willebrand factor (VWF) did not influence the risk of inhibitor formation (adjusted hazards ratio = 0.90). Lastly, the Rodin population study indicated that switching from a plasma-derived FVIII product (irrespective of relative VWF content) to a full-length rFVIII product did not increase the risk of inhibitor development. These conclusions Navitoclax are extremely cogent to patients and their physicians alike as the possibility that rFVIII products were more immunogenic, that the high content of VWF protein in plasma-derived FVIII products could protect against

alloantibody formation, and that product switching would be harmful all were used as rationale to determine the choice of replacement product for previously untreated, slightly previously treated, and even those previously treated individuals with over 150 exposure days. This published report notwithstanding the possibility that 上海皓元医药股份有限公司 it may be underpowered to conduct most of the above comparisons due to the relatively low number of patients treated with plasma-derived molecules has added to the cumulative published data, which tend to discount these concerns when determining product choice for previously untreated patients (PUPs) and others. In fact, several of the haemophilia treaters and haemophilia treatment centres (HTC), who participated in Rodin, had expressed publicly prior to this publication that

these same concerns influenced their decision to initiate their PUPs considered at higher risk for inhibitor development on plasma-derived products. The Rodin trial was observational, that is NOT a randomized controlled study, and allowed each HTC to determine independently how it was to treat its PUPs. This approach could have led to an imbalance in the baseline prognostic characteristics of the groups being compared in Rodin and this potential bias could have introduced a significant biostatical flaw into the study design [2]. In a post hoc analysis [1] and not apparently intended to be included in the original trial design [3], Gouw et al. compared the two generations of full-length rFVIII concentrates employed in the study for alloantibody inhibitor formation.

It is not clear whether the clearance of insulin is altered in li

It is not clear whether the clearance of insulin is altered in liver steatosis. Methods: This study was designed to observe the change of expression of

IDE in C57BL/6 mice with high fat diet-induced liver steatosis. Liver steatosis was induced in C57BL/6 mice via feeding with high fat diet for 16 weeks and the mice with chow diet as the control group. The hepatic protein and mRNA level of IDE were determined by western blot and RT-PCR. To make a compare, the intensity of the protein signal was analyzed quantitatively using Image J software. Results: Macroscopic and microscopic findings demonstrated that lipids were accumulated in the liver and liver steatosis was confirmed. Western blot showed that IDE was obviously higher in the high fat diet group that that in the control group (1 ± 0.17 vs 2.80 ± 0.24, p < 0.05). But the relative IDE mRNA level Y-27632 of the high fat diet induced

Vemurafenib research buy steatosis group was significantly lower than those in the control group (1 ± 0.09 vs 0.35 ± 0.05, p < 0.05). The decreased expression of IDE mRNA may be a compensation for the increased expression of IDE protein level. Conclusion: IDE is increased in mice with high fat diet induced liver steatosis. Key Word(s): 1. insulin degrading; 2. liver steatosis; Presenting Author: LILI YUAN Additional Authors: RUI ZHANG, NA ZHU, PING CAO Corresponding Author: LILI YUAN Affiliations: 上海皓元医药股份有限公司 Shanxi Dayu hospital Objective: There is a need for

us to get some effective and noninvasive methods to detect liver steatosis, which is a factor of liver fibrosis. Ultrasonic controlled attenuation parameter (CAP) is devised to target liver steatosis, which is based on vibration control transient elastography (VCTE). In this work, liver steatosis is evaluated using the novel CAP. Methods: All 60 patients were received examinations of liver Ultrosound, serum liver enzymes, and Fibroscan for measurement of transient elastography (TE) and CAP. Literature shows E value of Fibroscan significantly correlated with liver fibrosis. Grades of steatosis were divided by four groups (S0, S1, S2 and S3) by using Fibroscan CAP, 245,299 and 321 were the cutoff values of S1, S2 and S3. Mild and moderate to severe fatty liver were divided by using Ultrasound. Results: With the grades of steatosis progress diagnosed by Fibroscan CAP, the CAP value was significantly elevated in late groups compared with their previous groups respectively (table 1, p < 0.05), but there is no difference between the two groups diagnosed by Ultrasonic. No correlation was found for liver enzymes with grade of steatosis diagnosed by both methods. The E value was significantly increased in S3 group compared with in S0, S1 groups (table1, p < 0.05), indicted that with liver steatosis worsen, liver fibrosis was progressed.

It is not clear whether the clearance of insulin is altered in li

It is not clear whether the clearance of insulin is altered in liver steatosis. Methods: This study was designed to observe the change of expression of

IDE in C57BL/6 mice with high fat diet-induced liver steatosis. Liver steatosis was induced in C57BL/6 mice via feeding with high fat diet for 16 weeks and the mice with chow diet as the control group. The hepatic protein and mRNA level of IDE were determined by western blot and RT-PCR. To make a compare, the intensity of the protein signal was analyzed quantitatively using Image J software. Results: Macroscopic and microscopic findings demonstrated that lipids were accumulated in the liver and liver steatosis was confirmed. Western blot showed that IDE was obviously higher in the high fat diet group that that in the control group (1 ± 0.17 vs 2.80 ± 0.24, p < 0.05). But the relative IDE mRNA level Alpelisib clinical trial of the high fat diet induced

MG-132 clinical trial steatosis group was significantly lower than those in the control group (1 ± 0.09 vs 0.35 ± 0.05, p < 0.05). The decreased expression of IDE mRNA may be a compensation for the increased expression of IDE protein level. Conclusion: IDE is increased in mice with high fat diet induced liver steatosis. Key Word(s): 1. insulin degrading; 2. liver steatosis; Presenting Author: LILI YUAN Additional Authors: RUI ZHANG, NA ZHU, PING CAO Corresponding Author: LILI YUAN Affiliations: MCE公司 Shanxi Dayu hospital Objective: There is a need for

us to get some effective and noninvasive methods to detect liver steatosis, which is a factor of liver fibrosis. Ultrasonic controlled attenuation parameter (CAP) is devised to target liver steatosis, which is based on vibration control transient elastography (VCTE). In this work, liver steatosis is evaluated using the novel CAP. Methods: All 60 patients were received examinations of liver Ultrosound, serum liver enzymes, and Fibroscan for measurement of transient elastography (TE) and CAP. Literature shows E value of Fibroscan significantly correlated with liver fibrosis. Grades of steatosis were divided by four groups (S0, S1, S2 and S3) by using Fibroscan CAP, 245,299 and 321 were the cutoff values of S1, S2 and S3. Mild and moderate to severe fatty liver were divided by using Ultrasound. Results: With the grades of steatosis progress diagnosed by Fibroscan CAP, the CAP value was significantly elevated in late groups compared with their previous groups respectively (table 1, p < 0.05), but there is no difference between the two groups diagnosed by Ultrasonic. No correlation was found for liver enzymes with grade of steatosis diagnosed by both methods. The E value was significantly increased in S3 group compared with in S0, S1 groups (table1, p < 0.05), indicted that with liver steatosis worsen, liver fibrosis was progressed.