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| 1 | Elucidation of the ‘Honeycrisp’ pedigree through haplotype analysis with a multi-family integrated SNP linkage map and a large apple (Malus×domestica) pedigree-connected SNP data set显示文摘The apple(Malus×domestica)cultivar Honeycrisp has become important economically and as a breeding parent.An earlier study with SSR markers indicated the original recorded pedigree of‘Honeycrisp’was incorrect and‘Keepsake’was identified as one putative parent,the other being unknown.The objective of this study was to verify‘Keepsake’as a parent and identify and genetically describe the unknown parent and its grandparents.A multi-family based dense and high-quality integrated SNP map was created using the apple 8 K Illumina Infinium SNP array.This map was used alongside a large pedigree-connected data set from the RosBREED project to build extended SNP haplotypes and to identify pedigree relationships.‘Keepsake’was verified as one parent of‘Honeycrisp’and‘Duchess of Oldenburg’and‘Golden Delicious’were identified as grandparents through the unknown parent.Following this finding,siblings of‘Honeycrisp’were identified using the SNP data.Breeding records from several of these siblings suggested that the previously unreported parent is a University of Minnesota selection,MN1627.This selection is no longer available,but now is genetically described through imputed SNP haplotypes.We also present the mosaic grandparental composition of‘Honeycrisp’for each of its 17 chromosome pairs.This new pedigree and genetic information will be useful in future pedigree-based genetic studies to connect‘Honeycrisp’with other cultivars used widely in apple breeding programs.The created SNP linkage map will benefit future research using the data from the Illumina apple 8 and 20 K and Affymetrix 480 K SNP arrays. | Nicholas P Howard Eric van de Weg David S Bedford Cameron P Peace Stijn Vanderzande Matthew D Clark Soon Li Teh Lichun Cai James J Luby | 2017 | Horticulture Research2017，4，1： | 9 |
| 2 | Notch signaling controls chondrocyte hypertrophy via indirect regulation of Sox9显示文摘RBPjk-dependent Notch signaling regulates both the onset of chondrocyte hypertrophy and the progression to terminal chondrocyte maturation during endochondral ossification. It has been suggested that Notch signaling can regulate Sox9 transcription, although how this occurs at the molecular level in chondrocytes and whether this transcriptional regulation mediates Notch control of chondrocyte hypertrophy and cartilage development is unknown or controversial. Here we have provided conclusive genetic evidence linking RBPjk-dependent Notch signaling to the regulation of Sox9 expression and chondrocyte hypertrophy by examining tissuespecific Rbpjk mutant(Prx1Cre;Rbpjkf/f), Rbpjk mutant/Sox9 haploinsufficient(Prx1Cre;Rbpjkf/f;Sox9f/1),and control embryos for alterations in SOX9 expression and chondrocyte hypertrophy during cartilage development. These studies demonstrate that Notch signaling regulates the onset of chondrocyte maturation in a SOX9-dependent manner, while Notch-mediated regulation of terminal chondrocyte maturation likely functions independently of SOX9. Furthermore, our in vitro molecular analyses of the Sox9 promoter and Notch-mediated regulation of Sox9 gene expression in chondrogenic cells identified the ability of Notch to induce Sox9 expression directly in the acute setting, but suppresses Sox9 transcription with prolonged Notch signaling that requires protein synthesis of secondary effectors. | Anat Kohn Timothy P Rutkowski Zhaoyang Liu Anthony J Mirando Michael J Zuscik Regis J O'Keefe Matthew J Hilton | 2015 | Bone Research2015，3，3： | 8 |
| 3 | Metabolic and hepatic effects of liraglutide,obeticholic acid and elafibranor in diet-induced obese mouse models of biopsy-confirmed nonalcoholic steatohepatitis显示文摘AIM To evaluate the pharmacodynamics of compounds in clinical development for nonalcoholic steatohepatitis(NASH) in obese mouse models of biopsy-confirmedNASH.METHODS Male wild-type C57 BL/6 J mice(DIO-NASH) and Lep^(ob/ob)(ob/ob-NASH) mice were fed a diet high in trans-fat(40%), fructose(20%) and cholesterol(2%) for 30 and 21 wk, respectively. Prior to treatment, all mice underwent liver biopsy for confirmation and stratification of liver steatosis and fibrosis, using the nonalcoholic fatty liver disease activity score(NAS) and fibrosis staging system. The mice were kept on the diet and received vehicle, liraglutide(0.2 mg/kg, SC, BID), obeticholic acid(OCA, 30 mg/kg PO, QD), or elafibranor(30 mg/kg PO, QD) for eight weeks. Within-subject comparisons were performed on changes in steatosis, inflammation, ballooning degeneration, and fibrosis scores. In addition, compound effects were evaluated by quantitative liver histology, including percent fractional area of liver fat, galectin-3, and collagen 1 a1.RESULTS Liraglutide and elafibranor, but not OCA, reduced body weight in both models. Liraglutide improved steatosis scores in DIO-NASH mice only. Elafibranor and OCA reduced histopathological scores of hepatic steatosis and inflammation in both models, but only elafibranor reduced fibrosis severity. Liraglutide and OCA reduced total liver fat, collagen 1 a1, and galectin-3 content, driven by significant reductions in liver weight. The individual drug effects on NASH histological endpoints were supported by global gene expression(RNA sequencing) and liver lipid biochemistry.CONCLUSION DIO-NASH and ob/ob-NASH mouse models show distinct treatment effects of liraglutide, OCA, and elafibranor, being in general agreement with corresponding findings in clinical trials for NASH. The present data therefore further supports the clinical translatability and utility of DIO-NASH and ob/ob-NASH mouse models of NASH for probing the therapeutic efficacy of compounds in preclinical drug development for NASH. | Kirstine S Tolbol Maria NB Kristiansen Henrik H Hansen Sanne S Veidal Kristoffer TG Rigbolt Matthew P Gillum Jacob Jelsing Niels Vrang Michael Feigh | 2018 | World Journal of Gastroenterology2018，24，2： | 5 |
| 4 | N-acetylcysteine treats intravenous amiodarone induced liver injury显示文摘We report a case of intravenous(IV) amiodarone drug induced liver injury(DILI).The patient received IV N-acetylcysteine(NAC) which resulted in a rapid improvement in liver enzymes.While the specific mechanisms for the pathogenesis of IV amiodaroneDILI and the therapeutic action of IV NAC are both unknown, this case strongly implies at least some commonality.Because IV amiodarone is indicated for the treatment of serious cardiac arrhythmias in an intensive care unit setting, some degree of ischemic hepatitis is likely a cofactor in most cases. | Matthew L Mudalel Kartikeya P Dave James P Hummel Steven F Solga | 2015 | World Journal of Gastroenterology2015，21，9： | 5 |
| 5 | Proton pump inhibitors increase the severity of hepatic encephalopathy in cirrhotic patients显示文摘BACKGROUND Liver cirrhosis is the late stage of hepatic fibrosis and is characterized by portal hypertension that can clinically lead to decompensation in the form of ascites,esophageal/gastric varices or encephalopathy.The most common sequelae associated with liver cirrhosis are neurologic and neuropsychiatric impairments labeled as hepatic encephalopathy(HE).Well established triggers for HE include infection,gastrointestinal bleeding,constipation,and medications.Alterations to the gut microbiome is one of the leading ammonia producers in the body,and therefore may make patients more susceptible to HE.AIM To investigate the relationship between the use of proton pump inhibitors(PPIs)and HE in patients with cirrhosis.METHODS This is a single center,retrospective analysis.Patients were included in the study with an admitting diagnosis of HE.The degree of HE was determined from subjective and objective portions of hospital admission notes using the West Haven Criteria.The primary outcome of the study was to evaluate the grade of HE in PPI users versus non-users at admission to the hospital and throughout their hospital course.Secondary outcomes included rate of infection,gastrointestinal bleeding within the last 12 mo,mean ammonia level,and model for end-stage liver disease scores at admission.RESULTS The HE grade at admission using the West Haven Criteria was 2.3 in the PPI group compared to 1.7 in the PPI nonuser group(P=0.001).The average length of hospital stay in PPI group was 8.3 d compared to 6.5 d in PPI nonusers(P=0.046).Twenty-seven(31.8%)patients in the PPI user group required an Intensive Care Unit admission during their hospital course compared to 6 in the PPI nonuser group(16.7%)(P=0.138).Finally,10(11.8%)patients in the PPI group expired during their hospital stay compared to 1 in the PPI nonuser group(2.8%)(P=0.220).CONCLUSION Chronic PPI use in cirrhotic patients is associated with significantly higher average West Haven Criteria for HE compared to patients that do not use PPIs. | Matthew Fasullo Prashanth Rau Dong-Qi Liu Erik Holzwanger Jomol P Mathew Yurima Guilarte-Walker Gyongyi Szabo | 2019 | World Journal of Hepatology2019，11，6： | 4 |
| 6 | Proposed international clinical diabetic retinopathy and diabetic macular edema disease severity scales显示文摘 | C.P Wilkinson Frederick L Ferris Ronald E Klein Paul P Lee Carl David Agardh Matthew Davis Diana Dills Anselm Kampik R Pararajasegaram Juan T Verdaguer | 2003 | Ophthalmology2003，，9： | 4 |
| 7 | 多年生黑麦草、雀麦根系形态和生长对土壤干旱的适应性显示文摘为了研究牧草根系对干旱环境的适应性,选择多年生黑麦草(Lolium perenne)和雀麦(Bromus valdivianus)进行盆栽试验,给予80%~85%有效水(PAW)充分供水和20%~25%PAW极端干旱两种水分模式,通过对两种牧草的根系外形、干物质积累和根系形态学分析,探求两牧草在极干旱胁迫下的有效生产策略。研究表明,两种牧草的根尖外形略有不同。雀麦根毛长而密,分生区细胞致密,伸长区较长;多年生黑麦草根毛稀疏,伸长区短。20%~25%PAW极干旱胁迫使黑麦草根系粗细不匀,出现畸形;而雀麦根系未见明显受害。两种牧草生物量在茎叶和根的积累无显著的种间差异和水分处理间的组间差异。雀麦和多年生黑麦草单株根系的总长度、根面积、根平均直径、根尖数和分叉数存在极显著差异。多年生黑麦草根量显著高于雀麦(至少P≤0.01),根长和面积是雀麦的1.5倍左右,根尖数和分叉数是雀麦的2倍以上。雀麦根系末端侧根分枝密度高,短且粗;多年生黑麦草侧根细而长。干旱胁迫显著减少了两种牧草的总根长度,促进了雀麦根的径向生长。总之,雀麦根毛区较多年生黑麦草发达,多年生黑麦草根量显著多于雀麦。黑麦草主要以根数量(量)取胜,采取广泛吸水的适应策略;雀麦以根毛发达,侧根分枝密度高(质)为主,采用确保有效吸水的适应策略。 | 张咏梅 胡海英 白小明 Matthew Cory García-Favre Javier Ordóñez Iván P | 2022 | 中国生态农业学报(中英文)2022，30，11： | 3 |
| 8 | Sodium glucose co-transporter 2 inhibition reduces succinate levels in diabetic mice显示文摘BACKGROUND Type 1 diabetes(T1D) is associated with major chronic microvascular complications which contribute significantly to diabetes associated morbidity.The protein primarily responsible for glucose reabsorption in the kidney is sodium glucose co-transporter 2(SGLT2). Presently, SGLT2 inhibitors are widely used in diabetic patients to improve blood glucose levels and prevent cardiovascular and renal complications. Given the broad therapeutic application of SGLT2 inhibitors, we hypothesised that SGLT2 inhibition may exert its protective effects via alterations of the gut microbiome and tested this in a type 1 diabetic mouse model of diabetic retinopathy.AIM To determine whether the treatment with two independent SGLT2 inhibitors affects gut health in a type 1 diabetic mouse model.METHODS The SGLT2 inhibitors empagliflozin or dapagliflozin(25 mg/kg/d) or vehicle dimethylsulfoxide(DMSO) were administered to C57 BL/6 J, Akita, Kimba and Akimba mice at 10 wk of age for 8 wk via their drinking water. Serum samples were collected and the concentration of succinate and the short chain fatty acid(SCFA) butyric acid was measured using gas chromatography-mass spectrometry. Enzyme-linked immunosorbent assay(ELISA) was performed to determine the concentration of insulin and leptin. Furthermore, the norepinephrine content in kidney tissue was determined using ELISA. Pancreatic tissue was collected and stained with haematoxylin and eosin and analysed using brightfield microscopy.RESULTS Due to the presence of the Akita allele, both Akita and Akimba mice showed a reduction in insulin production compared to C57 BL/6 J and Kimba mice.Furthermore, Akita mice also showed the presence of apoptotic bodies within the pancreatic islets. The acinar cells of Akita and Akimba mice showed swelling which is indicative of acute injury or pancreatitis. After 8 wk of SGLT2 inhibition with dapagliflozin, the intermediate metabolite of gut metabolism known as succinate was significantly reduced in Akimba mice when compared to DMSO treated mice. In addition, empagliflozin resulted in suppression of succinate levels in Akimba mice. The beneficial SCFA known as butyric acid was significantly increased in Akita mice after treatment with dapagliflozin when compared to vehicle treated mice. The norepinephrine content in the kidney was significantly reduced with both dapagliflozin and empagliflozin therapy in Akita mice and was significantly reduced in Akimba mice treated with empagliflozin.In non-diabetic C57 BL/6 J and Kimba mice, serum leptin levels were significantly reduced after dapagliflozin therapy.CONCLUSION The inhibition of SGLT2 reduces the intermediate metabolite succinate, increases SCFA butyric acid levels and reduces norepinephrine content in mouse models of T1 D. Collectively, these improvements may represent an important mechanism underlying the potential benefits of SGLT2 inhibition in T1 D and its complications. | Lakshini Y Herat Natalie C Ward Aaron L Magno Elizabeth P Rakoczy Marcio G Kiuchi Markus P Schlaich Vance B Matthews | 2020 | World Journal of Gastroenterology2020，26，23： | 3 |
| 9 | Macrophage secretory products induce an inflammatory phenotype in hepatocytes显示文摘AIM:To investigate the influence of macrophages on hepatocyte phenotype and function.METHODS:Macrophages were differentiated from THP-1 monocytes via phorbol myristate acetate stimulation and the effects of monocyte or macrophageconditioned medium on HepG2 mRNA and protein expression determined.The in vivo relevance of these findings was confirmed using liver biopsies from 147 patients with hepatitis C virus(HCV)infection.RESULTS:Conditioned media from macrophages,but not monocytes,induced a transient morphological change in hepatocytes associated with upregulation of vimentin(7.8±2.5-fold,P=0.045)and transforming growth factor(TGF)-β1(2.6±0.2-fold,P<0.001)and downregulation of epithelial cadherin(1.7±0.02-fold,P=0.017)mRNA expression.Microarray analysis revealed significant upregulation of lipocalin-2(17-fold,P <0.001)and pathways associated with inflammation,and substantial downregulation of pathways related to hepatocyte function.In patients with chronic HCV,realtime polymerase chain reaction and immunohistochemistry confirmed an increase in lipocalin-2 mRNA(F0 1.0 ±0.3,F1 2.2±0.2,F2 3.0±9.3,F3/4 4.0±0.8,P= 0.003)and protein expression(F1 1.0±0.5,F2 1.3± 0.4,F3/4 3.6±0.4,P=0.014)with increasing liver injury.High performance liquid chromatography-tandem mass spectrometry analysis identified elevated levels of matrix metalloproteinase(MMP)-9 in macrophageconditioned medium,and a chemical inhibitor of MMP-9 attenuated the change in morphology and mRNA expression of TGF-β1(2.9±0.2 vs 1.04±0.1,P<0.001) in macrophage-conditioned media treated HepG2 cells.In patients with chronic HCV infection,hepatic mRNA expression of CD163(F0 1.0±0.2,F1/2 2.8±0.3,F3/4 5.3±1.0,P=0.001)and MMP-9(F0 1.0±0.4,F1/2 2.8±0.3,F3/4 4.1±0.8,P=0.011)was significantly associated with increasing stage of fibrosis.CONCLUSION:Secreted macrophage products alter the phenotype and function of hepatocytes,with increased expression of inflammatory mediators,suggesting that hepatocytes actively participate in liver injury. | Michelle Melino Victoria L Gadd Gene V Walker Richard Skoien Helen D Barrie Dinesh Jothimani Leigh Horsfall Alun Jones Matthew J Sweet Gethin P Thomas Andrew D Clouston Julie R Jonsson Elizabeth E Powell | 2012 | World Journal of Gastroenterology2012，18，15： | 3 |
| 10 | Senescent human hepatocytes express a unique secretory phenotype and promote macrophage migration显示文摘AIM:To develop a model of stress-induced senescence to study the hepatocyte senescence associated secretory phenotype(SASP).METHODS:Hydrogen peroxide treatment was used to induce senescence in the human Hep G2 hepatocyte cell line.Senescence was confirmed by cytochemical staining for a panel of markers including Ki67,p21,heterochromatin protein 1β,and senescence-associated-β-galactosidase activity.Senescent hepatocytes were characterised by gene expression arrays and quantitative polymerase chain reaction(q PCR),and conditioned media was used in proteomic analyses,a human chemokine protein array,and cell migration assays to characterise the composition and function of the hepatocyte SASP.RESULTS:Senescent hepatocytes induced classical markers of senescence(p21,heterochromatin protein1β,and senescence-associated-β-galactosidase activity);and downregulated the proliferation marker,Ki67.Hepatocyte senescence induced a 4.6-fold increase in total secreted protein(P=0.06)without major alterations in the protein profile.Senescence-induced genes were identified by microarray(Benjamini Hochbergcorrected P<0.05);and,consistent with the increase in secreted protein,gene ontology analysis revealed a significant enrichment of secreted proteins among inducible genes.The hepatocyte SASP included characteristic factors such as interleukin(IL)-8 and IL-6,as well as novel components such as SAA4,IL-32and Fibrinogen,which were validated by q PCR and/or chemokine protein array.Senescent hepatocyteconditioned medium elicited migration of inflammatory(granulocyte-macrophage colony stimulating factor,GM-CSF-derived),but not non-inflammatory(CSF-1-derived)human macrophages(P=0.022),which could contribute to a pro-inflammatory microenvironment in vivo,or facilitate the clearance of senescent cells.CONCLUSION:Our novel model of hepatocyte senescence provides insights into mechanisms by which senescent hepatocytes may promote chronic liver disease pathogenesis. | Katharine M Irvine Richard Skoien Nilesh J Bokil Michelle Melino Gethin P Thomas Dorothy Loo Brian Gabrielli Michelle M Hill Matthew J Sweet Andrew D Clouston Elizabeth E Powell | 2014 | World Journal of Gastroenterology2014，20，47： | 2 |
| 11 | Computational Identification of Plant MicroRNAs and Their Targets, Including a Stress-Induced miRNA显示文摘 | Matthew W Jones-Rhoades David P Bartel | 2004 | Molecular Cell2004，，6： | 2 |
| 12 | Procedural complexity independent of P2Y12 reaction unit(PRU)values is associated with acute in situ thrombosis in Pipeline flow diversion of cerebral aneurysms显示文摘background Acute in situ thrombosis is an ischaemic phenomenon during Pipeline embolisation device(PED)procedures with potentially high morbidity and mortality.There is controversy regarding the role of platelet function testing with P2Y12 assay as a predictor of intraprocedural thromboembolic events.There is limited knowledge on whether procedural complexity influences these events.Methods Data were collected retrospectively on 742 consecutive PED cases at a single institution.Patients with intraprocedural acute thrombosis were compared with patients without these events.results A cohort of 37 PED cases with acute in situ thrombosis(mean age 53.8 years,mean aneurysm size 8.4 mm)was matched with a cohort of 705 PED cases without intraprocedural thromboembolic events(mean age 56.4 years,mean aneurysm size 6.9 mm).All patients with in situ thrombosis received intra-arterial and/or intravenous abciximab.The two groups were evenly matched in patient demographics,previous treatment/subarachnoid hemorrhage(SAH)and aneurysm location.There was no statistical difference in postprocedural P2Y12 reaction unit(PRU)values between the two groups,with a mean of 156 in the in situ thrombosis group vs 148 in the control group(p=0.5894).Presence of cervical carotid tortuosity,high cavernous internal carotid artery grade,need for multiple PED and vasospasm were not significantly different between the two groups.The in situ thrombosis group had statistically significant longer fluoroscopy time(60.4 vs 38.4 min,p<0.0001),higher radiation exposure(3476 vs 2160 mGy,p<0.0001),higher rates of adjunctive coiling(24.3% vs 8.37%,p=0.0010)and higher utilisation of balloon angioplasty(37.8% vs 12.2%,p<0.0001).Clinically,the in situ thrombosis cohort had higher incidence of major and minor stroke,intracerebral haemorrhage and length of stay.Conclusions Predictors of procedural complexity(higher radiation exposure,longer fluoroscopy time,adjunctive coiling and need for balloon angioplasty)are associated with acute thrombotic events during PED placement,independent of PRU values. | Bowen Jiang Matthew T Bender Erick M Westbroek Jessica K Campos Li-Mei Lin Risheng Xu Rafael J Tamargo Judy Huang Geoffrey P Colby Alexander L Coon | 2018 | Stroke & Vascular Neurology2018，3，3： | 2 |
| 13 | Proposed international clinical diabetic retinopathy and diabetic macular edema disease severity scales显示文摘 | C.P Wilkinson Frederick L Ferris Ronald E Klein Paul P Lee Carl David Agardh Matthew Davis Diana Dills Anselm Kampik R Pararajasegaram Juan T Verdaguer | 2003 | Ophthalmology2003，，9： | 2 |
| 14 | Nutrient budgets in intensive shrimp ponds:implications for sustainability显示文摘 | MATTHEW R P | 1998 | Aquaculture1998，，： | 1 |
| 15 | Homeostasis model assessment:insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man显示文摘 | Matthews D R Hosker J P Rudenski A S | 2002 | Diabetes Care2002，25，10： | 1 |
| 16 | Tumorigenesissuppressor Pdcd4 dow n-regulates mitogen-activated pro-tein kinase 1 expression to suppress colon carcinoma cellinvasion显示文摘 | Yang H S Matthews C P Clair T | 2006 | Mol Cell Biol2006，26，4： | 1 |
| 17 | Cloning and mapping of variety-speeific rice genomic DNA sequences:amplifled fragment length polymorphisms(AFLP)from silver-stained Polyaerylamide gels显示文摘 | Yong G C MattheW w B OliVier P et a1 | 1996 | Genome1996，39，： | 1 |
| 18 | Continuity of kinetics between sub-and supercritical regimes in the oxidation of a high-volatile solid substrate显示文摘 | JONES J C CHIZ P S KOH R MATTHEW J | 1996 | Fuel1996，75，15： | 1 |
| 19 | Evaluation of the biocompatibility of a chitosan scaffold in mice显示文摘 | vander Vord P J Matthew H W DeSilva S P et aI | 2002 | Biomed Mater Res2002，59，3： | 1 |
| 20 | Adaptation of HIV-1to human leukocyte antigen class I显示文摘 | Kawashima Y Pfafferott K Frater J Matthews P Payne R Addo M Gatanaga H Fujiwara M Hachiya A Koizumi H Kuse N Oka S Duda A Prendergast A Crawford H Leslie A Brumme Z Brumme C Allen T Brander C Kaslow R Tang J Hunter E Allen S Mulenga J Branch S Roach T John M Mallal S Ogwu A Shapiro R Prado J G Fidler S Weber J Pybus O G Klenerman P Ndung'u T Phillips R Heckerman D Harrigan P R Walker B D Takiguchi M Goulder P | 2009 | Nature2009，458，7238： | 1 |
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