Total nucleic acid was extracted from leaf tissues and subjected to reverse transcription polymerase chain reaction (RT-PCR) using Hop stunt viroid (HSVd) and Citrus exocortis viroid (CEVd)-specific primers, followed by sequencing of PCR products. RT-PCR with HSVd primers amplified a 302- or 305-bp product from affected samples, but none from healthy plants. CEVd was not detected in affected trees. HSVd was also found in graft- and mechanically

inoculated plants. Sequence analyses showed three variants of HSVd in symptomatic mulberries related to plum and peach variants of this viroid with 94.9% identity, but with only 93% identity to Lebanese and Italian mulberry isolates. This is the first report of HSVd associated with vein clearing in mulberry in Iran. “
“Brown eye spot, Inhibitor Library research buy caused by Cercospora coffeicola, Selleckchem Maraviroc is an important disease of coffee. Both adaxial and abaxial leaf surfaces were inoculated with a conidial suspension of C. coffeicola. Samples were collected from 4 to 168 h after inoculation and then again at 35 days. Germinated conidia showed positive tropism to stomata where attempted penetrations occurred. Appressoria were not observed. After penetration, C. coffeicola colonized the lacunous parenchyma both inter and intracellularly. Sporulation occurred through or

around the stomata. Results from this study provide new insights into the infection process of C. coffeicola on coffee leaf. “
“Alfalfa fields in three western provinces of Iran were surveyed for Peanut stunt virus (PSV) during 2011 and 2012. Forty-seven of 115 samples tested (41%) were infected with PSV. Phylogenetic analysis using coat protein (CP) gene sequences showed that the Iranian isolates belong to the subgroup II of PSV. Pairwise identity analysis revealed four groups representing

four medchemexpress phylogenetic subgroups. PSV strains in subgroups III and IV are closely related to each other, as supported by the lowest nucleotide diversity, high pairwise nucleotide identity and high haplotype diversity as evidence of a recent population expansion after a genetic bottleneck. Using the maximum likelihood method, amino acid 86S in the CP gene of the Iranian PSV isolates was found to be under positive selection, although the likelihood ratio test statistics is not significant. This is the first report of the occurrence and phylogenetic relationships of Iranian PSV isolates in west Iran. “
“Gummy stem blight (GSB) is one of the most destructive foliar diseases of cucurbits, worldwide. To identify and characterize the pathogen which causes GSB on watermelon and muskmelon in East China, morphological characteristics, pathogenicity assays as well as sequence characterization of the rDNA internal transcribed spacer (ITS) were performed on 41 isolates collected from Jiangsu, Zhejiang, Anhui and Jiangxi provinces.

Dr Ishii proved biochemically and immunohistochemically that chronic alcohol consumption stimulated adaptive proliferation of the smooth endoplasmic reticulum in hepatocytes, and this increases metabolism of ethanol and other drugs, thereby explaining both tolerance to ethanol and increased hepatotoxicity of various drugs, anesthetics, and carcinogens. Several important medications, such as anticoagulants and sedatives, show decreased effectiveness

in alcoholics because of this increased microsomal CYP2E1 activity. This remarkable finding is a fine tribute to his http://www.selleckchem.com/products/Fulvestrant.html work as an investigator. Dr Ishii returned to the Division of Gastroenterology, Keio University School of Medicine in 1972, where he rose through the ranks to become Professor of Internal Medicine in 1994. Dr Ishii incorporated the strong scientific basis for medicine Alvelestat nmr as his two great predecessors, Professor Ken Sanbe and Professor Masaharu Tsuchiya, in addition to Professor Lieber, and in turn, ensured these principles were carried over to his own students; they still run deeply in his successors. Dr Sanbe’s concept was that the liver plays a central role among systemic organ interactions, while Dr Tsuchiya believed that gastrointestinal and liver diseases

are neuro-immunohormonal manifestations of systemic disorders. Dr Ishii’s great accomplishment was that he developed their theories microscopically and macroscopically. He led the Gastroenterology Division

of Keio, one of the most prominent university hospitals in Japan, and contributed greatly to consolidate the robust scientific and clinical status presently renowned worldwide. With his strong investigative mind and broad experience as a physician–scientist, he influenced the training and careers of more than 100 researchers and doctors. The number of papers presented both internationally and domestically every year from Ishii and his group was enormous. In his lifetime, he published over 1000 original papers in English and Japanese, and dozens of books. He traveled internationally more than 100 times for academic purposes. In fact, it might be that Professor Ishii spoke abroad as an invited lecturer more times than any other Japanese gastroenterologist. He worked vigorously in many important leading positions in many scientific groups, including 上海皓元医药股份有限公司 Deputy Director General of the Japan Society of Hepatology, and a committee member of the Ministry of Health, Labor, and Welfare. He was known as an Editor-in-Chief of the Journal of Gstroenterology and Hepatology, an official publication of Asian–Pacific Association of Gstroenterology, and also an Editor-in-Chief of Hepatology Research, the official journal of the Japan Society of Hepatology. Further, he was an Associate Editor of Alcoholism: Clinical and Experimental Research, the official journal of Research Society of Alcohol, USA (RSoA).

1a) without infiltration of inflammatory mononuclear cells. Hepatic triglyceride content was measured to quantify the degree of steatosis. The triglyceride Autophagy Compound Library content was significantly greater in OVX transgenic mice than in mice in the other three groups (Fig. 1b),

which was consistent with the results for hepatic steatosis. Thus, the increase in the serum ALT level in the OVX transgenic mice was thought to reflect the hepatic steatosis. Only OVX transgenic mice showed marked hepatic steatosis, regardless of the comparable diet intake and the ratio of liver to bodyweight of OVX non-transgenic mice (Table 1). We have previously demonstrated that iron-overloaded male FL-N/35 transgenic mice expressing the HCV polyprotein develop severe hepatic steatosis SRT1720 chemical structure through increased ROS production.[11] Therefore, we examined

whether ROS production was relevant to the marked hepatic steatosis observed in the OVX transgenic mice. Ovariectomy significantly increased ROS (superoxide) production in both transgenic mice and non-transgenic mice, but the level of ROS production was greater in the OVX transgenic mice than in the OVX non-transgenic mice (Fig. 2). We next measured inflammatory cytokine levels in the liver. Ovariectomy significantly increased hepatic expression of IL-6 mRNA to the same degree in both transgenic mice and non-transgenic mice (Fig. 3). This ovariectomy-induced increase in hepatic IL-6 mRNA was consistent with the results of a previous report that OVX mice produced more hepatic IL-6 than non-OVX mice after chemically induced liver injury.[5] There also was a trend for increase in TNF-α and IL-1β mRNA expression after ovariectomy in both the transgenic mice and non-transgenic mice, but their increases did not reach statistical significance, probably because of the large deviation (Fig. 3). These results suggested that inflammatory

cytokines were unlikely to be associated with greater ROS production in OVX transgenic mice than in OVX non-transgenic mice. We previously reported that male MCE公司 FL-N/35 transgenic mice developed hepatic iron accumulation through the reduced transcription of hepcidin,[18] a negative regulator in iron homeostasis.[21, 22] Excess divalent iron can be highly toxic, mainly via the Fenton reaction producing hydroxyl radicals.[23] Therefore, we measured hepatic iron content to assess whether greater ROS production resulted from increased hepatic iron accumulation in OVX transgenic mice. Unexpectedly, ovariectomy significantly decreased hepatic iron content to the same degree in both transgenic mice and non-transgenic mice (Fig. 4a). These results are potentially explained by significantly increased transcription of hepcidin after ovariectomy (Fig. 4b).

The technology for substituting the essential genes which these viruses require for replication and capsid formation by

therapeutic DNA was developed by many researchers including James Wilson, Katherine Selinexor mw High and Judah Samulski [3,4]. Very good results with factor IX DNA contained in AAV vectors were reported in mice and dogs with haemophilia. There was no toxicity and life-time correction of bleeding tendency was achieved. It proved harder to get similar results in early clinical (i.e. in human) trials. Muscle injection of factor IX gene containing AAV vector was only transiently effective [5] in elevating the plasma factor IX level. A subsequent trial with a similar vector administered into the hepatic artery was briefly effective in one subject of the seven treated, Selleckchem XAV-939 who achieved a factor IX level of 12%. However, the transfected liver cells were eliminated by a brisk T-cell immune response to vector capsid with consequent fall of factor IX level to base line by 8 weeks after vector infusion [6]. Building on this work an Anglo-American team at St Jude Children’s research hospital and University College London developed a new more potent vector which could be given by peripheral vein infusion based on a self-complementary design as well as codon optimization of the modified factor IX gene. Extensive tests in mice and

monkeys showed this to be both safe and up to 100 times more effective [7,8] than comparable vectors. As the factor IX gene is contained in a version of the virus that homes to the liver (AAV8) it was possible to administer the vector by infusion into a limb vein. With long-term

data from preclinical studies using the new vector, permission was sought to initiate a trial in patients with severe haemophilia B. The clinical trial protocol was designed primarily to assess safety, and secondly to find the minimum dose of vector required to elevate the subjects’ factor IX level from less than 1% to over 3%. medchemexpress Approval was given by the FDA and by the MHRA and GTAC committees (the relevant agencies controlling clinical trials in the USA and UK respectively) early in 2010. Since a detailed interim report of this trial has been published [9], a brief overview and update will be given herein. The first six patients to enter the trial were recruited in London and treated over the next 12 months at minimum intervals of 6 weeks. Subjects had to be over 18 with severe haemophilia B, no evidence of inhibitors, negative for hepatitis C RNA and HIV and with normal liver function. They also had to take part in an extensive informed consent process at two levels. At the first level, the trial is outlined and the likely risks explained so that informed consent to be tested for eligibility can be given. After testing, about half of the volunteers were eligible to proceed and the rest had to be deferred. The commonest reason for deferral was the presence of antibodies to the vector serotype AAV8.

35, 95% CI: 1.09-26.33, p = 0.039) Key Word(s): 1. Helicobacter pylori; 2. eradication; 3. idiopathic thrombocytopenic purpura; 4. platelet count Presenting Author: TAKUMA KAGAMI Additional Authors: MITSUSHIGE SUGIMOTO, SHU SAHARA, HITOMI ICHIKAWA, TAKAHISA FURUTA Corresponding Author: TAKUMA KAGAMI Affiliations: Hamamatsu University School of Medicine, Hamamatsu University School of Medicine, Hamamatsu University School

of Medicine, Hamamatsu Bafilomycin A1 in vitro University School of Medicine Objective: Recent studies have indicated that the eradication of H. pylori improves the histological gastric atrophy. However, there are no reports on the long-term observation of endoscopic changes of gastric atrophy and its expansion after eradication of H. pylori. We investiga ted the long-term effect of H. pylori eradication on the gastric mucosal atrophy assessed by endoscopy. Methods: Thirty-eight patients who underwent

gastroscopy every 1-3 years after eradication of H. pylori from1998 to 2003 were retrospectively studied. Gastric mucosal atrophy was endoscopically assessed according to the Kimura – Takemoto classification system and scored f rom 0 to 6 corresponding to C-0 (no atrophy), C-I, C-II, C-III, O-I, O-II, and O-III of the system, respectively . Endoscopic atrophy before eradication were also graded into mild (1-2), moderate (3-4) and severe atrophy (5-6). Follow up PKC412 in vitro periods were divided to pre-eradication, the early (1–5 years after eradication), middle (6-9 years), and late (10∼15 years) periods. Successive changes in scores for endoscopic atrophy before and after eradication were analyzed. Results: The median of atrophy score was significantly decreased from 3.5 to 3.5 (early: P = 0.023), 3 (middle: P <0.001) and 2 (late: P < 0.001) after eradication. When stratified based on the atrophic grades before eradication therapy, decreases in the score for atrophy was more evident in the mild atrophy group in comparison with the intermediate and severe groups. Conclusion: Eradication of

H. pylori infection improved gastric mucosal atrophy assessed by endoscopy during the long-term period, especially in the patients with mild atrophy. Key Word(s): 1. gastric atrophy H. pylori Presenting Author: HODONG KIM Additional Authors: SEUNG CHOI, JAEWON BEOM Corresponding Author: HODONG KIM Affiliations: Saint Carollo Hosipital, Saint Carollo Hosipital Objective: To MCE evaluate a new monoclonal antibody for the urease of Helicobacter pylori in gastric tissue biopsy specimens from humans by an immunochromatographic assay. Methods: One hundred seven volunteers were enrolled in the study. All of the subjects underwent a 13C-urea breath test (UBT) before esophagogastroduodenoscopy. Gastric aspirates were analyzed for pH and ammonia. Six biopsy specimens in the gastric antrum and body were obtained for a rapid urease test (RUT) and histology. Positive results for two of UBT, histology, and RUT confirmed H. pylori infection.

8 These factors

suggest that if IL28B genotyping is used, it should be considered along with other baseline predictors of response and virological status at week 4. An attractive scenario is that patients with favorable IL28B genotyping but HCV genotype 1 virus may be able to reduce treatment time from 48 weeks. click here Although this issue is a priority of future studies, at this time, there is insufficient data to recommend shortening the duration of standard of care. Another clinical advance is the recent identification of two inosine triphosphatase (ITPA) polymorphisms known to be functionally responsible for ITPA deficiency and strongly protective against RBV-induced hemolytic anemia.24 ITPA genotyping could help guide clinical decision-making, especially for patients in whom treatment with RBV is avoided or relatively contraindicated because of the high risk for developing anemia. It is unclear whether IL28B genotyping will be relevant in the context of direct antiviral therapy. The effects of IL28B genotype appear to be most substantial during the first phase of viral decline. PD98059 chemical structure Therefore, direct antivirals that have swift, potent effects on viral load may diminish the influence of IL28B genotyping in predicting SVR. However, direct antivirals achieve reductions in viral load by a variety of mechanisms, and it should not be assumed that IL28B genotyping

will have the same implications with different therapies or treatment strategies. The lack of data regarding 上海皓元 whether IL28B genotype is predictive of response when directly acting antivirals are added

to IFN and RBV makes a definitive statement on combination treatment difficult. Knowledge of IL28B’s effect in patients taking directly acting antivirals is a priority for research and clinical care. Both the process of IL28B genotyping and the possibility of tailored therapy affect the pharmacoeconomics of hepatitis C therapy. An important consideration regarding IL28B genotyping is whether it will be covered by health care plans. Coverage of genotyping could enhance clinical decision-making. However, coverage of treatment should not be based on genotyping alone. It is hoped that clinical and patient advocacy groups will insist that IL28B status is not used to deny treatment, especially given that its informative value is not absolute. In the context of drug development, tailored therapy has several potential implications. Segmenting the treatment population may reduce the overall size of the market; however, this may not necessarily limit profit. Throughout the world, treatment for HCV has poor patient uptake, often because of patient concerns about efficacy and tolerability. Pharmacogenetics could make a drug more appealing to a specific group of patients, such as African Americans with a C/C genotype at rs12979860.

39 Interestingly, PF-derived myofibroblasts secrete large amounts of the TGF-β isoform TGF-β2 and express high levels of the selleck screening library TGF-β receptor betaglycan, which is required for high-affinity signaling by TGF-β2.40 Combined with evidence that damaged BDE in human tissue express TGF-β2 and release inflammatory mediators (discussed below), this suggests a model whereby BDE damage leads to initial PF myofibroblastic differentiation, followed by autocrine perpetuation of the process.41 The impact of other growth factors on the function of PFs is less clear. Tumor necrosis factor-α, although up-regulated in patients with advanced

primary biliary cirrhosis,42 has not been shown to regulate PF activity, and our unpublished data suggest that it has no effect on PF myofibroblastic differentiation or type I collagen production. Similarly, the role of connective tissue growth factor in PF biology has not yet been studied, although it often enhances or mediates the effects of TGF-β and is up-regulated in human biliary fibrosis and in animal

models of chronic liver disease.43, Selleckchem MK-8669 44 Conflicting results have been reported for platelet-derived growth factor (PDGF). One group demonstrated that PDGF up-regulated α-SMA expression in PFs in culture; in rats subjected to BDL, injections of the protein-tyrosine kinase inhibitor ST1571 resulted in decreased α-SMA expression without altering bile ductular proliferation.17 Another

group, however, observed that PDGF enhanced PF proliferation in culture but decreased α-SMA expression.22 PDGF is of particular interest given that it is expressed by cultured bile duct segments from BDL-treated rats, suggesting 上海皓元医药股份有限公司 a possible mechanism for fibrosis after BDL.45 Interestingly, PDGF induces production of sonic hedgehog by myofibroblastic HSCs, which enhances HSC growth in an autocrine fashion.46 Although the role of hedgehog has not been studied in PFs, the hedgehog pathway is activated in rat livers after BDL, raising the possibility that PFs also produce or respond to hedgehog ligands.47 Strong evidence suggests that signals between BDE and PFs are instrumental in the progression of biliary fibrosis and cirrhosis. Several investigators have shown that there is a direct correlation between the intensity of the ductular reaction and the severity of fibrosis in human liver disease of a variety of etiologies, including hepatitis C and nonalcoholic fatty liver disease, as well as in animal models.16, 48-50 Cytokines and chemokines, in particular IL-6 and monocyte chemotactic protein-1 (MCP-1), are emerging as important mediators of cell–cell communication between BDE and PFs.

70, P < 0.007), they also moved more persistently (Z = 3.33, P < 0.001). Only 27% selleckchem of the infected snails, in contrast to 61% of the control ones, remained stationary during the whole observation period. The snails that actually moved did so in various

directions, often drawing convoluted lines, sometimes going back and forth, sometimes making circles. The effect of infection on alteration of the snail behaviour as expressed by the alteration index Ia(d), widely varied: the activity level was not affected (0); the tendency to stay in the cover (0.7) or in lighter places (0.9) was moderately altered. The strongest affected traits were the height above the ground (1.5) and mobility (3.2). The expression of the particular altered traits was to a large extent independent of one another (rs = 0.08–0.36, P > 0.05), only the snails staying higher in the vegetation tended to be in stronger illuminated places (rs = 0.56,

P < 0.002). Our observations revealed that the snails with pulsating L. paradoxum broodsacs behaved differently from their apparently non-infected counterparts. The infected snails differed in all measured traits but the activity level. Moreover, all these changes in the snail behaviour would be beneficial for the parasite. High mobility, combined with dwelling in the well-lit, exposed places, would increase the snails' visibility (detectability) to their potential definite hosts, that is, visually oriented birds. Simultaneously, their habit of staying on the upper surface of leaves, high in the vegetation, would increase their accessibility to the same group of potential hosts. So positioned snails could be approached and attacked R788 clinical trial from the air, the birds would not have to land and move through dense vegetation to pick the broodsacs. Thus, the observed behavioural changes fulfil the criteria of behavioural manipulation (Poulin, 2010), that is, it seems justifiable to claim that, additionally to its own phenotypic modifications (production of colourful pulsating broodsacs), L. paradoxum manipulates also the behaviour of its intermediate S. putris Telomerase host. Our findings agree with those of Wesenberg-Lund

(1931) on a related species, L. perturbatum (also infecting S. putris), in that the parasitized snails used to stay in well-illuminated places, on the upper parts of leaves. They sharply differ, though, in respect of the mobility patterns. Wesenberg-Lund (1931) found that ‘the parasitized snails are extremely sluggish in all their movements’, whereas our data show that the infected snails were much more mobile – actually this was the strongest affected variable of all. We are unable to say whether the divergence between the two studies is due to the real biological interspecific differences or, it rather stems from methodological differences: we observed the snails for short periods, while Wesenberg-Lund generalizations are based on long-term research.

Hepatic CIDEC mRNA levels were correlated positively with hepatic steatosis, the disease severity (MELD and ABIC score, HVPG), and mortality in AH patients. In conclusion, this long-term chronic plus binge ethanol feeding model partially

simulates the histo-logical and molecular features of human AH. FSP27/CIDE-C plays a critical role in promoting steatosis and hepatocellular damage in long-term chronic plus binge ethanol-fed mice and in human AH. Disclosures: Jim Lu – Employment: GoPath Pathology Associates, SC; Independent Contractor: GoPath Laboratories LLC; Management Position: GoPath Global LLC Ramon Bataller – Advisory Committees or Review Panels: Sandhill; Consulting: VTI The following people have nothing to disclose: Ming-Jiang Xu, Yan Cai, Jose T. Altamirano, Binxia Chang, Hua Wang, Adeline Bertola, Gemma Odena, Kimi-hiko click here Talazoparib purchase Matsusue, Shioko Kimura, Frank J. Gonzalez, Bin Gao BACKGROUND: Alcoholic and nonalcoholic fatty liver disease (ALD and NAFLD) commonly occur

in overweight or obese subjects (OW-OB). The impact of etiology on the intestinal micro-biome in the background of OW-OB is not known. AIMS: To compare the intestinal microbiome of OW-OB ALD to healthy controls and subjects with nonalcoholic fatty liver (NAFL) and nonalcoholic steatohepatitis (NASH), and their relationship to markers of liver injury. METHODS: Fecal 16S pyrosequenc-ing was performed on subjects with ALD, NAFL, NASH or weight-matched controls without fatty liver disease. The abundance of microbiota were compared using partial least squares discriminant analysis, parametric and nonparametric multiple group testing. Multiple regression analyses were used to relate liver injury markers to microbiota. RESULTS: Ninety eight subjects enrolled in total (mean BMI in kg/m2) – control, n=21 (26.7±5.3), NAFL, n=25

(32.5±5.3), NASH, n=35 (34.2±4.1) and ALD, n=17 (31.9±9) were studied. Microbial abundance : (a) Increased in ALD: Phyla : Proteobacteria (p< 0.008), Class: Firmicutes_Bacilli and Proteobacteria_Gammaproteobacteria (p< 0.01-0.0001), Order: Bifidobacteriales (p=0.01 vs. NAFL, 0.004 vs. NASH), Lactobacillales (p=0.02 vs. control and NASH), Enterobacteriales Terminal deoxynucleotidyl transferase (p=0.003 vs. control, p=0.0001 vs. NAFL and NASH), Family: Bifidobacteriaceae (p<0.01 both NAFL and NASH), Enterobacteriaceae (p=0.003 vs. control, p=0.0001 vs. NAFL and NASH), and Genus: Bifidobacterium (p=0.01 vs. NAFL, p=0.004 vs. NASH) and Escherichia/Shi-gella (p=0.008 vs. controls, p=0.016 vs. NAFL and p=0.009 vs. NASH). (b) Decreased in ALD: Phyla: Bacteroidetes (p=0.03 vs. NAFL, p=0.01 vs. NASH), Class: Bacteroidetes_Bacteroidia (p=0.03 vs. NAFL, p=0.01 vs. NASH) and Firmicutes_Clos-tridia (p=0.0023 vs. control, p=0.036 vs. NAFL and p=0.041 vs. NASH) (c) Changes in NAFLD: Only Actinobacteria had lower abundance in NASH vs. control (p=0.

Hepatic CIDEC mRNA levels were correlated positively with hepatic steatosis, the disease severity (MELD and ABIC score, HVPG), and mortality in AH patients. In conclusion, this long-term chronic plus binge ethanol feeding model partially

simulates the histo-logical and molecular features of human AH. FSP27/CIDE-C plays a critical role in promoting steatosis and hepatocellular damage in long-term chronic plus binge ethanol-fed mice and in human AH. Disclosures: Jim Lu – Employment: GoPath Pathology Associates, SC; Independent Contractor: GoPath Laboratories LLC; Management Position: GoPath Global LLC Ramon Bataller – Advisory Committees or Review Panels: Sandhill; Consulting: VTI The following people have nothing to disclose: Ming-Jiang Xu, Yan Cai, Jose T. Altamirano, Binxia Chang, Hua Wang, Adeline Bertola, Gemma Odena, Kimi-hiko Talazoparib cell line RAD001 order Matsusue, Shioko Kimura, Frank J. Gonzalez, Bin Gao BACKGROUND: Alcoholic and nonalcoholic fatty liver disease (ALD and NAFLD) commonly occur

in overweight or obese subjects (OW-OB). The impact of etiology on the intestinal micro-biome in the background of OW-OB is not known. AIMS: To compare the intestinal microbiome of OW-OB ALD to healthy controls and subjects with nonalcoholic fatty liver (NAFL) and nonalcoholic steatohepatitis (NASH), and their relationship to markers of liver injury. METHODS: Fecal 16S pyrosequenc-ing was performed on subjects with ALD, NAFL, NASH or weight-matched controls without fatty liver disease. The abundance of microbiota were compared using partial least squares discriminant analysis, parametric and nonparametric multiple group testing. Multiple regression analyses were used to relate liver injury markers to microbiota. RESULTS: Ninety eight subjects enrolled in total (mean BMI in kg/m2) – control, n=21 (26.7±5.3), NAFL, n=25

(32.5±5.3), NASH, n=35 (34.2±4.1) and ALD, n=17 (31.9±9) were studied. Microbial abundance : (a) Increased in ALD: Phyla : Proteobacteria (p< 0.008), Class: Firmicutes_Bacilli and Proteobacteria_Gammaproteobacteria (p< 0.01-0.0001), Order: Bifidobacteriales (p=0.01 vs. NAFL, 0.004 vs. NASH), Lactobacillales (p=0.02 vs. control and NASH), Enterobacteriales PtdIns(3,4)P2 (p=0.003 vs. control, p=0.0001 vs. NAFL and NASH), Family: Bifidobacteriaceae (p<0.01 both NAFL and NASH), Enterobacteriaceae (p=0.003 vs. control, p=0.0001 vs. NAFL and NASH), and Genus: Bifidobacterium (p=0.01 vs. NAFL, p=0.004 vs. NASH) and Escherichia/Shi-gella (p=0.008 vs. controls, p=0.016 vs. NAFL and p=0.009 vs. NASH). (b) Decreased in ALD: Phyla: Bacteroidetes (p=0.03 vs. NAFL, p=0.01 vs. NASH), Class: Bacteroidetes_Bacteroidia (p=0.03 vs. NAFL, p=0.01 vs. NASH) and Firmicutes_Clos-tridia (p=0.0023 vs. control, p=0.036 vs. NAFL and p=0.041 vs. NASH) (c) Changes in NAFLD: Only Actinobacteria had lower abundance in NASH vs. control (p=0.