Standard statistical analyses were performed using JMP selleck products 7.0.2 or SAS version 9.1 software (both from SAS Institute, Inc). IP-10 concentrations were log-transformed before use in statistical tests to meet distribution normality assumptions. Publicly available packages in R (version 2.8.0) were used to assess different classification models (diagonal linear discriminant analysis, random forest, support vector

machine, and bagging), as well as receiver operating characteristic (ROC) curve analysis. Fitting of logistic regression models and generalized linear models was performed using the proc logistic and procgenmod procedures, respectively, in SAS. Graphs were made using the above-mentioned statistical software or with GraphPad Prism 4 (GraphPad Software, Inc). All data are presented as the mean ± SD. Serum samples from 157 responders and 115 nonresponders to antiviral therapy were included selleck from the VIRAHEP-C cohort for this study. The definitions of responder and nonresponder are provided in Patients and Methods. Patients with viral relapse, breakthrough, or <12 weeks of available virological data were excluded. The cohort consisted of 134 AA and 138 CA patients. Baseline

patient characteristics of this cohort were as follows: age, 48.4 ± 7.4 years; viral load, 4.6 ± 5.7 × 106 IU/mL; platelet count, 214 ± 73 × 106 cells/mm3; alanine aminotransferase, 90.9 ± 72.9 IU/L; selleck screening library total bilirubin, 0.70 ± 0.35 mg/dL; albumin, 4.1 ± 0.40 g/dL; and hematocrit, 43.2 ± 3.8 % (Supporting Table 1). The cohort included 96 females and 176 males, and 19% with an Ishak fibrosis score of 4-6. Samples from 210 of the 272 patients in our cohort were available for IL28B genotyping (123 responders and 87 nonresponders), of whom 111 were CA and 99 were AA. Mean serum IP-10 levels were significantly lower in responders versus nonresponders (437

± 31 pg/mL versus 704 ± 44 pg/mL, P< 0.001) (Fig. 1A, Table 1). To assess the potential predictive value of IP-10 measurements, we stratified the patients according to a 600 pg/mL threshold value that has been used in other studies.15, 16, 18 Sixty-nine percent (129/188) of patients with a low baseline IP-10 level (<600 pg/mL) were responders (positive predictive value, 69%), whereas 67% (56/83) of patients with a high baseline IP-10 level (>600 pg/mL) were nonresponders (negative predictive value, 67%) (Fig. 1B). Overall, this results in a specificity of 82% (129/157) and a sensitivity of 49% (56/115) for a test predictive of therapy response based on pretreatment serum IP-10 levels. Baseline demographic parameters of the cohort stratified according to pretreatment IP-10 level are shown in Supporting Table 1. Between high and low IP-10 groups, significant differences were seen for several parameters, implying a possible association with IP-10 level. Previous groups have also noted association of race and viral load with IP-10 levels.

6 ± 71.6 days). On multivariate analysis, remaining stones during stenting treatment was significantly associated with a higher rate LDK378 purchase of MPD restenosis (p = 0.03). Conclusion: EPS is an effective and useful procedure and useful for prevention of re-stricture in patients with benign pancreatic duct strictures from severe stricture and ESWL assist cases. Key Word(s): 1. Endoscopic Pancreatic Stenting long term results chronic pancreatitis Presenting Author: EISUKE IWASAKI Additional Authors: YOSHIYUKI YAMAGISHI, SHINTARO KAWASAKI, TAKASHI SEINO, MISAKO MATSUCHITA,

HAJIME HIGUCHI, JUNTARO MATSUZAKI, NAOKI HOSOE, KAZUHIRO KASHIWAGI, MAKOTO NAGANUMA, HIDEKAZU SUZUKI, TAKANORI KANAI, HARUHIKO OGATA Corresponding Author: EISUKE IWASAKI Affiliations: Keio University School of Medicine, Keio University School of Medicine, Keio XL765 solubility dmso University School of Medicine, Keio University School of Medicine, Kitasato University Kitasato Institute Hospital, Keio University School of Medicine, Keio University School of Medicine, Keio University School of Medicine, Keio University School of Medicine, Keio University School of Medicine, Keio University

School of Medicine, Keio University School of Medicine Objective: The endoscopic intervention in the management of walled-off pancreatic necrosis (WOPN) has been developed recently. Endoscopic necrosectomy (EN) for WOPN is less invasive

than surgical treatment. Our purpose was to report our experience of EN. Methods: Three patients with a WOPN which occured despite performed continuous regional arterial infusion of a protease inhibitor and antibiotic for severe acute pancreatitis, received EN. Case 1 was a 72-year-old woman with WOPN from the gallstone pancreatitis. Case 2 was a 49-year-old man with WOPN from severe alcoholic pancreatitis. Case 3 was a 43-year-old woman with WOPN from severe necrotic pancreatitis with severe general condition on prolonged ventilator. Results: The number of EN session was six in case 1, two in case 2 and one in case 3. All three patients achieved clinical Unoprostone remission and resume a normal life. The abscess were completely disappeared in both case 1 and 2. Only in case 3, EN was not effective for WOPN because of the presence of a fistula to descending colon. She finally required surgery. Procedure related complications were occurred in all patients, minor bleeding in case1 and 3, and minor perforation in case 2 which were self-limiting under the conservative management. All patients are completely recovered and resume a normal life. Conclusion: In the present three cases with WOPN, EN was efficiently performed for the WOPN except in the presence of fistula to intestine. Key Word(s): 1. necrosectomy; 2.

29 Thus, the matrix chemistry transitions from its start point in the stem cell

niche having labile matrix Selleck ICG-001 chemistry associated with high turnover and minimal sulfation to stable matrix chemistries and having increasing amounts of sulfation with progression towards the pericentral zone. We hypothesize that maintenance of the natural architecture and matrix chemistry correlating with histology will facilitate recellularization in tissue engineering processes by guiding cells to specific sites on the biomatrix scaffolds and/or providing the proper mix of signals to drive differentiation into mature cells. The biomatrix scaffolds can be prepared from any tissue, normal or diseased, and from any species. In the supplement we show biomatrix scaffolds from human pancreas, biliary tree, and duodenum and from rat pancreas (Supporting Figs. S6-S9). Figures 5–7 and Supporting Fig. S5 show effects of bovine or rat liver biomatrix scaffolds on hepatic cells. In addition, biomatrix scaffolds have been prepared from human abdominal aorta, iliac vein,

and from rat and pig intestine (data not shown). Histological, ultrastructural, and immunohistochemical studies on the biomatrix scaffolds suggested a marked tissue specificity, but not species specificity, in their structure, chemical composition, and functions (data not shown). Plating hHpSCs onto dishes with sections of liver biomatrix scaffolds and in HDM tailored for adult liver cells resulted in essentially 100% of the viable cells attached within a few hours onto http://www.selleckchem.com/products/mitomycin-c.html biomatrix scaffolds, whether intact or after cryogenic pulverization. The colonies of cells that initially formed on the sections of scaffolds retained some of their stem cell phenotype, as the cells in the center of the colonies

were able to resist staining with dyes (Supporting Fig. S4) and expressed classic hepatic progenitor markers, such as chemokine (C-X-C motif) receptor 4 (CXCR4) and epithelial cell adhesion molecule (EpCAM) (Fig. 5E). They divided once or twice and then transitioned into cell cycle arrest and into 3D cord-like morphologies typical for cultures of mature parenchymal cells (Figs. 5, 6 for stem cells differentiation; compare with Fig. 7 and Supporting Fig. S5 for maintenance of GBA3 mature hepatocytes). The HDM used did not require all the usual cytokines or growth factors because these are present bound to the biomatrix scaffolds. The transition to growth arrest correlated with staining throughout the colonies with viability dyes (Supporting Fig. S4), with loss of expression of EpCAM and CXCR4 (Fig. 5E) and with a steady increase in the expression of adult-specific hepatocytic and cholangiocytic genes such as urea and cytochrome P450 3A4 (Fig. 5F). Normal adult rat and human hepatocytes were plated onto type I collagen versus on biomatrix scaffolds from rat or bovine livers and into HDM for adult cells.

The presence of iron may additionally contribute the reactive oxygen species, which can allow further progression of the disease. In summary, the findings reported in this study suggest that hepatic iron loading increases the synthesis and deposition of cholesterol in the liver. The mechanism appears to be independent of Srebf2. The observations are consistent with a role for iron in the development of NAFLD, with iron contributing, first, to increased cholesterol production and, second, to increased oxidative stress leading to lipid peroxidation. We are grateful to Mary Anne Townsend and the staff at PathWest Laboratory

Medicine Napabucasin mw WA, Fremantle Hospital, for performing the total cholesterol measurements. Additional Supporting Information may be found in the online version of this article. “
“Development of hepatic steatosis and its progression to steatohepatitis may be the consequence of dysfunction of several metabolic pathways, such as triglyceride synthesis, very low-density lipoprotein (VLDL) secretion, and fatty acid β-oxidation. Peroxisome proliferator-activated receptor γ coactivator-1β (PGC-1β) is a master regulator of mitochondrial biogenesis and oxidative metabolism, lipogenesis, and triglyceride (TG) secretion.

Here we generated a novel mouse model with constitutive hepatic activation of PGC-1β and studied the role of this transcriptional coactivator in dietary-induced steatosis and steatohepatitis. Selective activation of PGC-1β within hepatocytes is able to protect the liver from lipid overload and from progression to fibrosis. The protective function exerted by PGC-1β is due to its ability to induce selleck chemical mitochondrial oxidative phosphorylation, fatty acid β-oxidation, and citrate cycle, as well as to decrease oxidative stress and promote TG secretion in the blood stream. These findings bolster the concept that a combined hepatic specific action of PGC-1β on lipid synthesis and secretion, as well as on mitochondrial

biogenesis and function, could protect against steatohepatitis. (HEPATOLOGY 2013) Nonalcoholic fatty liver disease (NAFLD) is becoming a master component of the epidemic of obesity and metabolic syndrome worldwide due to excessive caloric intake.1 The spectrum Mephenoxalone of NAFLD ranges from simple fatty liver with benign prognosis to a potentially progressive form, nonalcoholic steatohepatitis (NASH), which may lead to liver fibrosis and cirrhosis resulting in increased morbidity and mortality. The initial phase of the steatosis or fatty liver is characterized by accumulation of fat droplets within the cytoplasm of a hepatocyte. Although simple steatosis is generally an asymptomatic syndrome with a benign course, it may progress through the inflammatory phase of steatohepatitis. Indeed, some cases develop a necroinflammatory state, hepatocytes ballooning with Mallory’s hyaline, and sometimes fibrosis, features that could result in cirrhosis and, in some patients, hepatocellular carcinoma.

The regional ethical committees of the three countries approved the clinical studies, and all patients had given written informed consent. Patients were included in the current analysis if they were of Scandinavian origin, infected

with HCV genotype 3, had been treated per protocol (>11 weeks of treatment with >80% of prescribed dose of both drugs, a follow-up sample was available to assess SVR), and had available stored plasma sample (n = 281, Fig. 1). Genomic DNA was extracted from 200 μL of frozen plasma samples using MagNA Pure LC Total Nucleic Acid Isolation Kit High Performance (Roche, Mannheim, Germany), DNA was eluted in 100 μL of elution buffer. Prior selleck screening library to initiating the study, we tested to see if there was sufficient amount of DNA extracted from plasma for genotyping without whole-genome Selleckchem Palbociclib amplification (WGA). WGA was found to be not necessary. Norwegian healthy controls were selected from the Norwegian Bone Marrow registry. Genomic DNA from controls was extracted from peripheral blood and thereafter amplified using the Genomiphi kit (GE Healthcare Systems, Chalfont St. Giles, UK), giving high-molecular amplified DNA previously validated for genotyping.20 Patients were treated with PEG-IFN-α-2b (PegIntron; Schering Plough, Kenilworth, NJ) 1,5 μg/kg subcutaneously once weekly and ribavirin (Rebetol; Schering

Plough) 800-1400 mg/day based on body weight (<65 kg: 800 mg/day; 65-85 kg: 1000 mg/day; 86-105 kg: 1200 mg; and >105 kg: 1400 mg/day). In both trials, Patients C59 molecular weight were considered to have RVR if they were RNA-negative (<50 IU/mL) after 4 weeks of treatment. In the nonrandomized trial, all patients with RVR were treated for a total of 14 weeks, whereas in the RCT trial, patients with RVR were randomized

to either 14 weeks or 24 weeks of total treatment. Patients without RVR were treated for 24 weeks in both trials. Patients were considered to have SVR if HCV RNA levels remained undetectable 24 weeks after completion of treatment. Qualitative HCV RNA analysis, viral load determination, and HCV genotyping for these patients have been described.18, 19 Liver biopsies were only available from a subset of patients from the nonrandomized trial. Liver fibrosis was therefore assessed using the aspartate aminotransferase platelet ratio index (APRI).21 An APRI of >1.5 was classified as bridging fibrosis or cirrhosis (stage 3-4), and hepatocyte injury was assessed by ALT measurements.22 Eluted DNA (5 μL) was used for determination of genotype using an SDS 7900 HT qPCR thermocycler (Applied Biosystems, Foster City, CA). rs12979860 was genotyped using a custom made TaqMan assay with the following primers and probes: amplification primers TGCCTGTCGTGTACTGA ACCA and GAGCGCGGAGTGCAATTC and TaqMan probes VIC-TGGTTCGCGCCTTC-MGB and 6FAM-CTGGTTCACGCCTTC-MGB.

Intrahepatic lipid accumulation plays a pathogenic role in liver injury in response to chronic ethanol exposure.[1] Lipin-1 plays an important role in regulating lipid metabolism by way of its cytoplasmic and nuclear effects.[5-7] In the present study, we provide evidence demonstrating that hepatic lipin-1 deficiency led to dramatically pronounced changes in terms of steatosis, inflammation, and fibrosis in response to chronic ethanol administration compared

to WT mice. This suggests that the buy LBH589 induction in lipin-1 in alcoholic fatty liver disease may play a protective role by limiting inflammation, promoting efficient lipid storage, and/or controlling the transcriptional regulation of fatty acid

catabolism. Correlating closely with the rapid onset and progression of steatosis and inflammation, hepatic PGC-1α abundance was found to be severely diminished in ethanol-fed lipin-1LKO mice leading to reduced expression of several PGC-1α target genes encoding fatty acid oxidation enzymes, decreased rates of hepatic fatty acid oxidation, reduced generation of ketone bodies, and impaired VLDL secretion. These findings can be interpreted to suggest that the loss nuclear lipin-1 leads to these deleterious effects since lipin-1 is known to regulate these processes at the transcriptional level.[5-7, 10] Indeed, lipin-1α overexpression suppressed alcohol-induced TG accumulation potentially by transcriptionally activating fatty acid catabolism. However, Selumetinib concentration it is possible that loss of lipin-1 enzymatic activity may somehow be affecting signaling pathways that lead to PGC-1α deactivation. For example, adipocyte-specific lipin-1 deletion led to impaired cAMP signaling in

that cell type,[15] and this pathway seems to be very important Amine dehydrogenase for regulation of PGC-1α in liver. Altogether, our results demonstrate that genetic ablation of hepatic lipin-1 aggravates experimental alcohol-induced steatohepatitis in mice. A marked increase in hepatic PAP activity has long been known to occur in alcoholic fatty liver in animals and humans.[2-4, 9] We have previously shown that lipin-1 is strongly induced in ethanol-induced fatty liver in mice and we sought to determine whether loss of lipin-1 would attenuate the increased PAP activity and intrahepatic triglyceride accumulation in response to ethanol feeding. Interestingly, our present study showed that removal of lipin-1 from the liver effectively abolished the increase in hepatic PAP activity caused by ethanol, but dramatically exacerbated ethanol-induced fatty liver in mice. Studies have demonstrated that fld mice display liver steatosis partly due to increased hepatic lipin-2-mediated PAP activity.

Intrahepatic lipid accumulation plays a pathogenic role in liver injury in response to chronic ethanol exposure.[1] Lipin-1 plays an important role in regulating lipid metabolism by way of its cytoplasmic and nuclear effects.[5-7] In the present study, we provide evidence demonstrating that hepatic lipin-1 deficiency led to dramatically pronounced changes in terms of steatosis, inflammation, and fibrosis in response to chronic ethanol administration compared

to WT mice. This suggests that the drug discovery induction in lipin-1 in alcoholic fatty liver disease may play a protective role by limiting inflammation, promoting efficient lipid storage, and/or controlling the transcriptional regulation of fatty acid

catabolism. Correlating closely with the rapid onset and progression of steatosis and inflammation, hepatic PGC-1α abundance was found to be severely diminished in ethanol-fed lipin-1LKO mice leading to reduced expression of several PGC-1α target genes encoding fatty acid oxidation enzymes, decreased rates of hepatic fatty acid oxidation, reduced generation of ketone bodies, and impaired VLDL secretion. These findings can be interpreted to suggest that the loss nuclear lipin-1 leads to these deleterious effects since lipin-1 is known to regulate these processes at the transcriptional level.[5-7, 10] Indeed, lipin-1α overexpression suppressed alcohol-induced TG accumulation potentially by transcriptionally activating fatty acid catabolism. However, selleckchem it is possible that loss of lipin-1 enzymatic activity may somehow be affecting signaling pathways that lead to PGC-1α deactivation. For example, adipocyte-specific lipin-1 deletion led to impaired cAMP signaling in

that cell type,[15] and this pathway seems to be very important Clomifene for regulation of PGC-1α in liver. Altogether, our results demonstrate that genetic ablation of hepatic lipin-1 aggravates experimental alcohol-induced steatohepatitis in mice. A marked increase in hepatic PAP activity has long been known to occur in alcoholic fatty liver in animals and humans.[2-4, 9] We have previously shown that lipin-1 is strongly induced in ethanol-induced fatty liver in mice and we sought to determine whether loss of lipin-1 would attenuate the increased PAP activity and intrahepatic triglyceride accumulation in response to ethanol feeding. Interestingly, our present study showed that removal of lipin-1 from the liver effectively abolished the increase in hepatic PAP activity caused by ethanol, but dramatically exacerbated ethanol-induced fatty liver in mice. Studies have demonstrated that fld mice display liver steatosis partly due to increased hepatic lipin-2-mediated PAP activity.

Intrahepatic lipid accumulation plays a pathogenic role in liver injury in response to chronic ethanol exposure.[1] Lipin-1 plays an important role in regulating lipid metabolism by way of its cytoplasmic and nuclear effects.[5-7] In the present study, we provide evidence demonstrating that hepatic lipin-1 deficiency led to dramatically pronounced changes in terms of steatosis, inflammation, and fibrosis in response to chronic ethanol administration compared

to WT mice. This suggests that the GSI-IX mw induction in lipin-1 in alcoholic fatty liver disease may play a protective role by limiting inflammation, promoting efficient lipid storage, and/or controlling the transcriptional regulation of fatty acid

catabolism. Correlating closely with the rapid onset and progression of steatosis and inflammation, hepatic PGC-1α abundance was found to be severely diminished in ethanol-fed lipin-1LKO mice leading to reduced expression of several PGC-1α target genes encoding fatty acid oxidation enzymes, decreased rates of hepatic fatty acid oxidation, reduced generation of ketone bodies, and impaired VLDL secretion. These findings can be interpreted to suggest that the loss nuclear lipin-1 leads to these deleterious effects since lipin-1 is known to regulate these processes at the transcriptional level.[5-7, 10] Indeed, lipin-1α overexpression suppressed alcohol-induced TG accumulation potentially by transcriptionally activating fatty acid catabolism. However, GSK3235025 chemical structure it is possible that loss of lipin-1 enzymatic activity may somehow be affecting signaling pathways that lead to PGC-1α deactivation. For example, adipocyte-specific lipin-1 deletion led to impaired cAMP signaling in

that cell type,[15] and this pathway seems to be very important GNE-0877 for regulation of PGC-1α in liver. Altogether, our results demonstrate that genetic ablation of hepatic lipin-1 aggravates experimental alcohol-induced steatohepatitis in mice. A marked increase in hepatic PAP activity has long been known to occur in alcoholic fatty liver in animals and humans.[2-4, 9] We have previously shown that lipin-1 is strongly induced in ethanol-induced fatty liver in mice and we sought to determine whether loss of lipin-1 would attenuate the increased PAP activity and intrahepatic triglyceride accumulation in response to ethanol feeding. Interestingly, our present study showed that removal of lipin-1 from the liver effectively abolished the increase in hepatic PAP activity caused by ethanol, but dramatically exacerbated ethanol-induced fatty liver in mice. Studies have demonstrated that fld mice display liver steatosis partly due to increased hepatic lipin-2-mediated PAP activity.

The main producers of liver collagen are myofibroblasts derived from activated hepatic stellate cells (HSCs). Additionally, other cell types, such as portal fibroblasts and bone marrow derived cells, may contribute to ECM production. Liver fibrosis develops on the basis of chronic liver injury induced, for example, by chronic viral hepatitis B or C infection, excessive alcohol abuse, or fatty liver

disease frequently associated with obesity.1 Although immune cells play an essential role in the modulation of liver fibrosis, its pathogenesis implicitly BGJ398 datasheet involves the injury and proliferation of HSC, hepatocytes, and, potentially, other cell species. Upon liver damage, dying hepatocytes stimulate remnant hepatocytes to reenter the cell cycle to restore original liver mass and function.2 Liver injury also stimulates HSC activation through complex mechanisms. This involves the conversion of a resting, vitamin A–storing cell into a proliferating HSC without vitamin A droplets, but is capable of producing proinflammatory cytokines and ECM components such as collagen.3 The transition from quiescent (i.e., G0) cells into the active phase of the cell cycle is predominantly controlled

by E-type cyclins and their associated kinase, cyclin-dependent kinase 2 (Cdk2).4 In mammals, two E-cyclins are known, termed cyclin E1 (CcnE1) and cyclin E2 (CcnE2), respectively.5, 6 Despite their anticipated essential function for developmental and regenerative processes, the single genetic inactivation of CcnE1, CcnE2, or Cdk2 does not check details affect viability or development in mice.7–10 However, fibroblasts deficient for both E-cyclins are unable to reenter the cell cycle from G0.9 We recently demonstrated that CcnE1 and CcnE2 play antagonistic roles in the regenerating liver after partial hepatectomy (PH).11 Accordingly, CcnE2−/− livers show increased, prolonged CcnE1/Cdk2 activity, resulting in earlier and sustained DNA synthesis, hepatomegaly, and excessive endoreplication

Janus kinase (JAK) of hepatocytes, whereas the ablation of CcnE1 provoked only a moderate delay of hepatocyte proliferation. Earlier work using rat HSCs indicated that HSC activation is associated with increased gene expression of CcnE, cyclin D, and induction of polyploidy.12 However, the precise role of E-type cyclins for the activation and proliferation of HSCs, and subsequent liver fibrogenesis, has remained elusive. In the present study, we aimed to investigate the contribution of E-type cyclins for liver fibrosis in vivo using constitutive CcnE1−/− and CcnE2−/− knock-out mice and derived primary HSCs. Our current work demonstrates that CcnE1, but not CcnE2, is essential for HSC survival, proliferation, and liver fibrogenesis.

In this work, we focus on (i) elucidating dynamics in root exudation of Solanum lycopersicum L. in an intercropping system due to AMF and/or Fol; (ii) its effect on Fol development

in vitro; and (iii) the testing of the root exudate compounds identified in the chromatographic analyses in terms of effects on fungal growth in in vitro assays. GC-MS analyses revealed an AMF-dependent increase in sugars and decrease in organic acids, mainly glucose and malate. In the HPLC analyses, an increase in chlorogenic acid Adriamycin mw was evident in the combined treatment of AMF and Fol, which is to our knowledge the first report about an increase in chlorogenic acid in root exudates of AM plants challenged with Fol compared

with plants inoculated with AMF only, clearly indicating changes in root exudation due to AMF and Fol. Root exudates of AMF tomato plants stimulate the germination rate of Fol, whereas the co-inoculation of AMF and Fol leads to a reduction in spore germination. In the in vitro assays, citrate and chlorogenic acid could be identified as possible candidates for the reduction in Fol germination rate in the root exudates of the AMF+Fol treatment because they proved inhibition at concentrations naturally occurring www.selleckchem.com/products/E7080.html in the rhizosphere. “
“To study the chemical composition of coffee beans from coffee cherries infected by brown eye spot, two experiments were conducted with coffee cherries from Catuaí Amarelo and Acaiá Cerrado farms, in the full physiological maturity stage. The coffee cherries were harvested manually, and 20 litres of cherries without

visible symptoms of brown eye spot (healthy coffee cherries) and 20 l of cherries with visible symptoms of the disease (diseased coffee cherries) were individually separated. After separation, the cherries were mixed in five different proportions to form the treatments: 0, 25, 50, 75 and 100% of diseased coffee cherries to 100, 75, 50, 25 and 0% of healthy coffee cherries. The experimental design was performed in randomized blocks, with each 8 l of coffee cherries being considered an experimental unit. After drying (humidity Fossariinae 12%), the chemical characteristics were analysed. Polyphenols, potassium leachate and electrical conductivity had a linear increase with the rising of the proportion of diseased coffee cherries. Total sugars, soluble solids and pH decreased linearly with the rising of the proportion of diseased coffee cherries. “
“Tomato (Solanum lycopersicum L.) is one of the most important vegetable crops in the world. However, the tomato production is severely affected by many diseases. The use of host resistance is believed to be the most effective approach to control the pathogens. In this study, a total of 1003 resistance-like genes were identified from the tomato genome using individual full-length search and conserved domain verification approach.