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Spontaneous bacterial peritonitis prevalence in pretransplant patients and its effect on survival and graft loss post-transplant

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World Journal of Hepatology 2016年第36期8卷 1617-1622页

作者： Neeral l Shah Nicolas M Intagliata Zachary H Henry Curtis K Argo Patrick G Northup Division of Gastroenterology and Hepatology Department of Medicine University of Virginia

AIM To investigate the incidence of spontaneous bacterial peritonitis(SBP) in pre-transplant patients and its effect on post transplant mortality and graft failure. METHODS We conducted a retrospective cohort study of patient records from the organ procurement and transplant network data set. Patients were identified by the presence of SBP pre-transplant. Univariate post-transplant survival models were constructed using the Kaplan-Meier technique and multivariate models were constructed using the cox proportional hazards model. Variables that affected post-transplant graft survival were identified in the SBP population. RESUlTS Forty-seven thousand eight hundred and eighty patient records were included in the analysis for both groups, and 1966(4.11%) patients were identified in the data set as having pre-transplant SBP. Patients that had pre-transplant SBP had higher rates of graft loss from recurrent hepatitis C virus(HCV)(3.6% vs 2.0%, P leading to graft loss(1.9% vs 1.3%, P = 0.02), primary non-function(4.3% vs 3.0%, P lan-Meier survival analysis showed a statistically significant difference in all-cause survival in patients with a history of SBP vs those without(P lant history of SBP was independently predictiveof mortality due to recurrent HCV(HR = 1.11, 95%CI: 1.02-1.21, P liver *** HCV patients prior to the advent of directing acting anti-viral agents had a higher incidence of pre-transplant SBP than other patients on the liver transplant wait list. SBP history pre-transplant resulted in a higher rate of graft loss due to recurrent HCV infection and chronic rejection.

关键词： Spontaneous bacterial peritonitis liver transplant Graft failure Hepatitis C

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Role of Protein Kinase Cδ-Mediated Spleen Tyrosine Kinase (Syk) Phosphorylation on Ser in the Amplification of Oral Mucosal Inflammatory Responses to Porphyromonas gingivalis

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Journal of Biosciences and Medicines 2018年第3期6卷 70-85页

作者： Bronislaw l.Slomiany Amalia Slomiany Research Center Rutgers School of Dental MedicineRutgersThe State University of New JerseyNewarkNJUSA

The signaling events underlying oral mucosal inflammatory responses to P. gingivalis and its key endotoxin, lipopolysaccharide (lPS), relay primarily on the lPS engagement of Toll-like receptor-4 (TlR4), and the activation of IκB-kinase complex (IKK) and mitogen-activated protein kinases (MAPKs that exert their control over transcription factors implicated in the regulation of iNOS and cox-2 proinflammatory genes expression). Since spleen tyrosine kinase (Syk) has emerged recently as a major amplifier in the production of proinflammatory mediators, we investigated the process of recruitment and interaction of Syk with TlR4 in salivary gland acinar cells in response to P. gingivalis lPS. Our findings revealed that stimulation of the acinar cells with the lPS leads to protein kinase Cδ (PKCδ)-mediated phosphorylation of Syk on Ser which results in its localization with the membrane associated TlR4 complex and the activation through phosphorylation on Tyr. Further, our results support the involvement of Syk in the amplification of transcription factors involved in the assembly and expression of transcription complexes associated with the induction in cox-2 and iNOS genes. Therefore, our data suggest that PKCδ is a primary linchpin affecting the Syk recruitment to the membrane localized TlR4, and hence affects the efficiency of the kinase activation and the magnitude of oral mucosal inflammatory response to P. gingivalis.

关键词： P. gingivalis Oral Mucosa PKCδ Syk Activation Ser/Tyr Phosphorylation

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Cytosolic phospholipase A2 S-nitrosylation in ghrelin protection against detrimental effect of ethanol cytotoxicity on gastric mucin synthesis ——Ghrelin in gastric mucosal protection

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Health 2010年第9期2卷 1033-1039页

作者： Bronislaw l. Slomiany Amalia Slomiany 不详

Ghrelin, a peptide hormone produced mainly in the stomach, has emerged recently as an important regulator of nitric oxide synthase (NOS) and cyclooxygenase (cox) enzyme systems, the products of which play direct cytoprotective function in the maintenance of gastric mucosal integrity. In this study, using gastric mucosal cells, we report on the role of ghrelin in countering the cytotoxic effect of ethanol on mucin synthesis. We show that the countering effect of ghrelin on mucin synthesis was associated with the increase in NO and PGE2 production, and characterized by a marked up-regulation in cytosolic phospholipase A2 (cPlA2) activity. The ghrelin-induced up-regulation in mucin synthesis, like that of cPlA2 activity, was subject to suppression by Src inhibitor, PP2 and ERK inhibitor, PD98059, as well as ascorbate. Moreover, the loss in countering effect of ghrelin on the ethanol cytotoxicity and mucin synthesis was attained with cNOS inhibitor, l-NAME as well as cox-1 inhibitor SC-560. The effect of l-NAME was reflected in the inhibition of ghrelin-induced mucosal cell capacity for NO production, cPlA2 S-nitrosylation and PGE2 generation, whereas cox-1 inhibitor caused only the inhibition in PGE2 generation. Our findings suggest that the activation of gastric mucosal cPlA2 through cNOS-induced S-nitrosylation plays an essential role in the countering effect of ghrelin on the disturbances in gastric mucin synthesis caused by ethanol cytotoxicity.

关键词： Ghrelin Ethanol Cytotoxicity Gastric Mucin CNOS CPlA2 S-Nitrosylation

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Cyclooxygenase-2 S-nitrosylation in salivary gland acinar cell inflammatory responses to Porphyromonas gingivalis: modulatory effect of ghrelin

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Advances in Bioscience and Biotechnology 2011年第6期2卷 434-442页

作者： Bronislaw l. Slomiany Amalia Slomiany 不详

Disturbances in nitric oxide synthase (NOS) system and the excessive prostaglandin (PGE2) generation are well-recognized features of oral mucosal inflammatory responses to periodontopathic bacterium, P. gingivalis. Employing rat sublingual gland acinar cells, we show that P. gingivalis lPS-induced up-regulation in PGE2 generation and the enhancement in inducible (i) iNOS activity was associated with cox-2 activation through S-nitrosylation, and accompanied by the suppression in cSrc activity and the impairment in constitutive (c) cNOS phosphorylation. Further, we demonstrate that the countering effect of peptide hormone, ghrelin, on the lPS-induced changes was reflected in the increased cNOS activation through phosphorylation, repression in iNOS induction, and the reduction in PGE2 generation associated with the loss of cox-2 protein S-nitrosylation. Moreover, the effect of ghrelin on cNOS phosphorylation and the lPS-induced cox-2 S-nitrosylation was susceptible to the blockage by cSrc inhibition. Our findings suggest that P. gingivalis-induced up-regulation in iNOS leads to cox-2 S-nitrosylation and up-regulation in PGE2 generation, and that the countering effect of ghrelin is mediated through Src-dependent cNOS activation that is obligatory for the maintenance of iNOS gene suppression.

关键词： Salivary Gland P. gingivalis iNOS Induction cox-2 Activation S-nitrosylation Ghrelin cNOS Phosphorylation

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Modulation of gastric mucosal inflammatory responses to Helicobacter pyloriby ghrelin: Role of cNOS-dependent IKK-βS-nitrosylation in the regulation of cox-2 activation

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American Journal of Molecular Biology 2012年第2期2卷 113-123页

作者： Bronislaw l. Slomiany Amalia Slomiany Research Center University of Medicine and Dentistry of New Jersey Newark USA

Disturbances in nitric oxide synthase (NOS) and cyclooxygenase (cox) isozyme systems, manifested by the excessive NO and prostaglandin (PGE2) generation, are well-recognized features of gastric mucosal inflammatory responses to H. pylori infection. In this study, we report that H. pylori lPS-induced enhancement in gastric mucosal inducible (i) iNOS expression and cox-2 activation was accompanied by the impairment in constitutive (c) cNOS phosphorylation, up-regulation in the inhibitory κB kinase-β (IKKβ) activation and the increase in the transcriptional factor, NF-κB, nuclear translocation. Further, we show that abrogation of cNOS control over NF-κB activation has lead to induction of iNOS expression and cox-2 activation through S-nitrosylation. Moreover, we demonstrate that the modulatory effect of peptide hormone, ghrelin, on the lPS-induced changes was reflected in the increase in Src/Akt-dependent cNOS activation through phosphorylation and the suppression of IKK-β activity through cNOS-mediated IKK-β protein S-nitrosylation. As a result, ghrelin exerted the inhibitory effect on NF-κB nuclear translocation, thus causing the repression of iNOS gene induction and the inhibition in cox-2 activation through iNOS-dependent S-nitrosylation. Our findings point to cNOS activation as a pivotal element in the signaling cascade by which ghrelin exerts modulatory control over proinflammatory events triggered in gastric mucosa by H. pylori infection.

关键词： H. pylori Gastric Mucosa iNOS Induction cox-2 Activation Ghrelin cNOS Phosphorylation IKK-β S-Nitrosylation

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Proinflammatory Signaling Cascades of Periodontopathic Oral Pathogen Porphyromonas gingivalis

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Journal of Biosciences and Medicines 2018年第5期6卷 63-88页

作者： Bronislaw l. Slomiany Amalia Slomiany Research Center Rutgers School of Dental Medicine Rutgers The State University of New Jersey Newark USA

Porphyromonas gingivalis, is the most prominent member of the bacteria flora associated with pathogenesis of periodontitis, a chronic inflammatory disease resulting in tooth loss. The extent of oral mucosal reaction to P. gingivalis invasion relays heavily on Toll-like receptors (TlRs) that recognize structurally common motifs of pathogens and initiate antibacterial responses. Among the virulence factors of P. gingivalis implicated in TlRs activation and triggering inflammatory responses leading to the development of periodontitis is the bacterium cell-wall lipopolysaccharide (lPS). The engagement by the lPS of oral mucosal TlR4 leads to initiation of signaling events characterized by the activation of mitogen-activated protein kinase (MAPK) and IκB-kinase complex (IKK) cascades, induction of phosphoinositide-specific phospholipase C (PlC)/protein kinase C (PKC)/PI3K pathway, up-regulation in TGF-α ectodomain shedding and EGFR transactivation, and the amplification of proinflammatory signals by spleen tyrosine kinase (Syk). These events, in turn, exert their control over transcription factors implicated in the induction of the expression of cyclooxygenase-2 (cox-2) and inducible nitric oxide synthase (iNOS) genes that lead to up-regulation in the inflammatory mediators, PGE2 and NO. The systems involved in transcription factors activation, furthermore, remain under additional regulatory control through S-nitrosylation. Moreover, the lPS-induced TlR4 activation provides a docking site for Syk, the activation of which leads to amplification of the inflammatory signals by affecting transcription factors activation and their assembly to transcriptional complexes. Interestingly, the extent of oral mucosal inflammatory response to P. gingivalis remains under modulatory influence by two biologically active peptide hormones, leptin and ghrelin. Therefore, the presence of these multifunctional peptides in oral mucosa and saliva may be of significance in countering the destru

关键词： P. gingivalis Periodontal Disease Oral Mucosa Inflammatory Response lPS TlR4 Signaling Cascades

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Role of constitutive nitric oxide synthase in regulation of Helicobacter pylori-induced gastric mucosal cyclooxygenase-2 ac-tivation through S-nitrosylation: mechanism of ghrelin action

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Open Journal of Gastroenterology 2011年第2期1卷 13-22页

作者： Bronislaw l. Slomiany Amalia Slomiany 不详

Gastric mucosal inflammatory responses to H. pylori lipopolysaccharide (lPS), are characterized by the excessive NO and prostaglandin (PGE2) generation due to the disturbances in nitric oxide synthase (NOS) and cyclooxygenase (cox) systems. Here, we report that the lPS-induced enhancement in gastric mucosal inducible (i) iNOS) activity and up-regulation in PGE2 production was associated with the suppression in Akt kinase activity and the impairment in constitutive (c) cNOS activation. The stimulatory effect of the lPS on PGE2 production, furthermore, was susceptible to suppression by cox-2 inhibitor, NS-398, and iNOS inhibitor, 1400 W. Further, we show that the countering effect of peptide hormone, ghrelin, on the lPS-induced changes was reflected in up-regu- lation in Akt activity and the increase in cNOS activation through phosphorylation, and accompanied by the suppression in iNOS expression and the reduction in cox-2 activity associated with the loss in cox-2 protein S-nitrosylation. Moreover, the effect of ghre-lin on the lPS-induced cox-2 S-nitrosylation was subject to repression by Akt inhibition. Our findings demonstrate that induction in iNOS with H. pylori in- fection leads to cox-2 activation through S-nitro- sylation and up-regulation in PGE2 generation, and that ghrelin counters these untoward consequences of the lPS through Akt-mediated up-regulation in cNO- S activation required for the iNOS gene repression.

关键词： H. pylori Gastric Mucosa iNOS Induction cox-2 Activation S-nitrosylation Ghrelin

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The N-terminus of cox-1 and its effect on cyclooxygenase-1 catalytic activity

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Journal of Genetics and Genomics 2010年第2期37卷 117-123页

作者： Sean Phipps Michael J. Turner Daniel l. Simmons Chemistry and Biochemistry Department Brigham Young University

Cyclooxygenases are encoded by cox-1 and cox-2. They share over sixty percent sequence identity in human and are similar to each other in their crystallographic structures. One major difference in the primary structure of these two isozymes is the presence of eight amino acids in the amino-terminal region of cox-1 that are not present in cox-2. The function of this amino acid sequence is unknown. In this study, a human cox-1 mutant （Δ7aa） with this sequence removed was studied in parallel with cox-1. Signal peptide cleavage, N-linked glycosylation, protein expression, distribution and dimerization were not affected by the mutation. The mutant was enzymati-cally active and showed the same sensitivity toward aspirin. The KM for the enzyme remained the same as cox-1. However, the Vmax of the cox-1 mutant decreased by 3.3-fold. We conclude that the cox-1 specific amino-terminal sequence has a subtle but detectable effect on cox-1 catalysis.

关键词： cox-1 cox-2 dimerization glycosylation aspirin KM Vmax

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增加日粮中小麦的比例对荷斯坦奶牛生产性能和瘤胃发酵的影响

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饲料与畜牧（新饲料） 2009年第8期 62-62页

作者：刘冰 l.Doepel A.cox A.Hayirli

12头处于第二次泌乳的荷斯坦奶牛，采用拉丁方设计研究增加日粮巾小麦比例对泌乳性能、瘤胃发酵和全肠养分消化率的影响。供试奶牛随机分为3组，分别饲喂0％、10％、20％蒸汽压片小麦（在干物质基础上替代等量蒸汽压片大麦）。每天饲喂... 详细信息

12头处于第二次泌乳的荷斯坦奶牛，采用拉丁方设计研究增加日粮巾小麦比例对泌乳性能、瘤胃发酵和全肠养分消化率的影响。供试奶牛随机分为3组，分别饲喂0％、10％、20％蒸汽压片小麦（在干物质基础上替代等量蒸汽压片大麦）。每天饲喂2次，挤奶2次。其中6头试验牛安装瘤胃瘘管，试验结束前2d采瘤胃液样本共计18次。不同处理的试验牛干物历摄入量（20．9kg／d）、产奶量（36．1kg／d）、乳成分（脂肪、蛋白、乳糖含量分别为1．25kg／d、1．10kg／d、1．67kg／d）差异不品著。

关键词：小麦奶牛消化率发酵

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New In Vitro Studies on the Bioprofile of Genista tenera Antihyperglycemic Extract

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Natural Products and Bioprospecting 2015年第6期5卷 277-285页

作者： Daniela Batista Pedro l.Falé Maria l.Serralheiro Maria E.Araújo Paulo J.A.Madeira Carlos Borges Isabel Torgal Margarida Goulart Jorge Justino Alice Martins Amélia P.Rauter Centro de Química e Bioquímica Faculdade de CiênciasUniversidade de LisboaCampo Grande1749-016 LisbonPortugal Institute of Pharmaceutical Science King’s College London150 Stamford StreetLondon SE19NHUK Escola Superior Agrária de Santarém Quinta do Galinheiro2001-904 SantarémPortugal

The inhibition of a-glucosidase and glucose-6-phosphatase,two enzymes involved in the carbohydrate metabolism,is an important target to control glycaemia on individuals with type 2 *** this work we report for the first time the inhibition of both enzymes by the antihyperglycemic n-butanol extract from Genista tenera(Fabaceae).This extract decreased a-glucosidase and glucose-6-phosphatase activities to 0.97 and 80.25%,respectively,being more effective than acarbose,and phlorizin,the positive controls,which reduced enzymes activities only to 17.39 and 96.06%.Once inflammation and oxidative stress are related to diabetic impairments,the anti-inflammatory activity of the extract was also evaluated,through its inhibitory activity over cox-1 enzyme(47.5%inhibition).Moreover,after induction of oxidative stress by UV radiation,the viability of irradiated rat liver hepatoma cells exposed to the extract was significantly higher(67.82%)than that promoted by ascorbic acid,the positive control(45.05%).In addition,the stability of the extract under gastrointestinal conditions was evaluated by HPlC–DAD-ESI–MS/*** diglycosides were identified as the main constituents of the extract,and no alterations in the chemical composition nor in the antioxidant activity were observed after in vitro digestion with artificial gastric and pancreatic juices.

关键词： a-Glucosidase inhibition In vitro digestion HPlC-DAD-ESI-MS/MS Antioxidant activity Flavonoid glycosides

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