Database : MEDLINE
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[PMID]: 29524531
[Au] Autor:Gong S; Lan T; Zeng L; Luo H; Yang X; Li N; Chen X; Liu Z; Li R; Win S; Liu S; Zhou H; Schnabl B; Jiang Y; Kaplowitz N; Chen P
[Ad] Address:State Key Laboratory of Organ Failure Research; Southern Medical University, Guangzhou, China; Guangdong Provincial Key Laboratory of Proteomics, Southern Medical University, Guangzhou, China; Department of Pathophysiology, Southern Medical University, Guangzhou, China.
[Ti] Title:Gut microbiota mediates diurnal variation of acetaminophen induced acute liver injury in mice.
[So] Source:J Hepatol;, 2018 Mar 07.
[Is] ISSN:1600-0641
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:BACKGROUND & AIMS: Acetaminophen (APAP) induced hepatotoxicity is a leading cause of acute liver failure worldwide. It is well established that the liver damage induced by acetaminophen exhibits diurnal variation. However, the detailed mechanism for the hepatotoxic variation is not clear. Here we aimed to determine the relative contributions of gut microbiota in modulating the diurnal variation of hepatotoxicity induced by APAP. METHODS: Male Balb/C mice were treated with or without antibiotics and orally administrated a single dose of APAP (300 mg/kg) at ZT0 (when the light is on-start of resting period) and ZT12 (when the light is off-start of active period). RESULTS: In agreement with previous findings, hepatic injury was markedly enhanced at ZT12 compared with ZT0. Interestingly, upon antibiotics treatment, ZT12 displayed protection against APAP hepatotoxicity similar to ZT0. Moreover, mice that received the cecal content from ZT12 showed more severe liver damage than mice that received the cecal content from ZT0. 16S sequencing data revealed significant differences in the cecal content between ZT0 and ZT12 in the compositional level. Furthermore, metabolomic analysis showed that the gut microbial metabolites were also different between ZT0 and ZT12. Specifically, the level of 1-phenyl-1,2-propanedione (PPD) was significantly higher at ZT12 than ZT0. Treatment with PPD alone did not cause obvious liver damage. However, PPD synergistically enhanced APAP induced hepatic injury in vivo and in vitro. Finally, we found Saccharomyces cerevisiae, which could reduce intestinal PPD levels, was able to markedly alleviate APAP induced liver damage at ZT12. CONCLUSIONS: The gut microbial metabolite, 1-phenyl-1,2-propanedione was responsible, at least in part, for the diurnal variation of hepatotoxicity induced by APAP by decreasing GSH levels. LAY SUMMARY: Acetaminophen (APAP) induced acute liver failure due to over dose is a leading public health problem. APAP induced liver injury exhibited diurnal variation, in particular, it causes more severe liver damage when taken at night compared with that in the morning. Here we showed that gut microbial metabolite, 1-phenyl-1,2-propanedione (PPD) is involved in the rhythmic hepatotoxicity induced by APAP by depleting hepatic GSH levels. Our data suggest gut microbiota may be a potential target for reducing APAP induced acute liver injury.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  2 / 396355 MEDLINE  
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[PMID]: 29524441
[Au] Autor:Bowness R; Chaplain MAJ; Powathil GG; Gillespie SH
[Ad] Address:School of Medicine, University of St Andrews, North Haugh, St Andrews, KY16 9TF, UK. Electronic address: rec9@st-andrews.ac.uk.
[Ti] Title:Modelling the effects of bacterial cell state and spatial location on tuberculosis treatment: Insights from a hybrid multiscale cellular automaton model.
[So] Source:J Theor Biol;, 2018 Mar 07.
[Is] ISSN:1095-8541
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:If improvements are to be made in tuberculosis (TB) treatment, an increased understanding of disease in the lung is needed. Studies have shown that bacteria in a less metabolically active state, associated with the presence of lipid bodies, are less susceptible to antibiotics, and recent results have highlighted the disparity in concentration of different compounds into lesions. Treatment success therefore depends critically on the responses of the individual bacteria that constitute the infection. We propose a hybrid, individual-based approach that analyses spatio-temporal dynamics at the cellular level, linking the behaviour of individual bacteria and host cells with the macroscopic behaviour of the microenvironment. The individual elements (bacteria, macrophages and T cells) are modelled using cellular automaton (CA) rules, and the evolution of oxygen, drugs and chemokine dynamics are incorporated in order to study the effects of the microenvironment in the pathological lesion. We allow bacteria to switch states depending on oxygen concentration, which affects how they respond to treatment. This is the first multiscale model of its type to consider both oxygen-driven phenotypic switching of the Mycobacterium tuberculosis and antibiotic treatment. Using this model, we investigate the role of bacterial cell state and of initial bacterial location on treatment outcome. We demonstrate that when bacteria are located further away from blood vessels, less favourable outcomes are more likely, i.e. longer time before infection is contained/cleared, treatment failure or later relapse. We also show that in cases where bacteria remain at the end of simulations, the organisms tend to be slower-growing and are often located within granulomas, surrounded by caseous material.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  3 / 396355 MEDLINE  
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[PMID]: 29516009
[Au] Autor:Bonomini F; Favero G; Rodella LF; Moghadasian MH; Rezzani R
[Ad] Address:Anatomy and Physiopathology Division, Department of Clinical and Experimental Sciences, University of Brescia, Viale Europa 11, 25123 Brescia, Italy.
[Ti] Title:Melatonin Modulation of Sirtuin-1 Attenuates Liver Injury in a Hypercholesterolemic Mouse Model.
[So] Source:Biomed Res Int;2018:7968452, 2018.
[Is] ISSN:2314-6141
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Hypercholesterolemia increases and exacerbates stress signals leading also to liver damage (LD) and failure. Sirtuin1 (SIRT1) is involved in lifespan extension and it plays an essential role in hepatic lipid metabolism. However, its involvement in liver hypercholesterolemic damage is not yet completely defined. This study evaluated the role of SIRT1 in the hypercholesterolemic-related LD and, then, investigated how oral supplementation of melatonin, pleiotropic indoleamine, may be protective. Control mice and apolipoprotein E-deficient mice (ApoE ) of 6 and 15 weeks of age were treated or not treated with melatonin at the dose of 10 mg/kg/day for 9 weeks. In this study, we evaluated serum biochemical markers, liver SIRT1 expression, and oxidative stress markers. We observed that hypercholesterolemia increased significantly serum cholesterol and triglycerides, reduced significantly liver SIRT1, and, in turn, induced hepatic oxidative stress in untreated ApoE mice with respect to control mice. Interestingly, melatonin treatment improved serum biochemical markers and hepatic morphological impairment and inhibited oxidative stress through its antioxidant properties and also by SIRT1 upregulation. In summary, melatonin oral supplementation may represent a new protective approach to block hypercholesterolemic liver alterations involving also a SIRT1-dependent mechanism.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Process
[do] DOI:10.1155/2018/7968452

  4 / 396355 MEDLINE  
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[PMID]: 29515749
[Au] Autor:Mirambo MM; Senyaeli N; Mshana SE
[Ad] Address:Department of Microbiology and Immunology, Weill Bugando School of Medicine, P.O. Box 1464, Mwanza, Tanzania.
[Ti] Title:Low humoral responses to human cytomegalovirus is associated with immunological treatment failure among HIV infected patients on highly active antiretroviral therapy.
[So] Source:Pan Afr Med J;28:131, 2017.
[Is] ISSN:1937-8688
[Cp] Country of publication:Uganda
[La] Language:eng
[Ab] Abstract:Human cytomegalovirus (HCMV) is one of the opportunistic infections associated with significant morbidity and mortality among HIV/AIDS patients especially before introduction of antiretroviral therapy (ART). Little is known regarding the humoral immune response against HCMV in relation to CD4 counts among HIV infected individuals. A total of 90 achieved sera from HIV infected patients attending Bugando Medical centre care and treatment centre (CTC) aged 18 years and above were retrieved and analyzed. Sociodemographic data were collected using structured data collection tool. Detection of specific HCMV antibodies was done using Indirect Enzyme Linked Immunosorbent Assay (ELISA). Data were analyzed by using STATA version 11. A total of 90 HIV infected patients were enrolled in the study whereby 36(40%) had immunological treatment failure. The mean age of the study participants was 39±12.3 years. The Prevalence of specific HCMV IgG antibodies was 84(93.3%, 95% CI: 88-98.5) while the prevalence of specific HCMV IgM antibodies was 2(2.3% 95% CI: 0.8-5.4). The median CD4 counts at 6 months and 12 months on HAART were significantly high in treatment success group. At 12 months of HAART as CD4 counts increases the HCMV IgG index value was also found to increase significantly, p=0.04. Significant proportion of HIV infected individuals was infected with HCMV. Higher median HCMV IgG titers were observed among patients with immunological treatment success. There is a need to investigate humoral immune responses in HIV infected individuals in relation to CD4 counts against various infectious diseases in developing countries where most of these infections are endemic.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Process
[do] DOI:10.11604/pamj.2017.28.131.10480

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[PMID]: 29515748
[Au] Autor:Aka KE; Apollinaire Horo G; Fomba M; Kouyate S; Koffi AK; Konan S; Fanny M; Effi B; Kone M
[Ad] Address:Department of Obstetrics and Gynecology, University Hospital of Yopougon, Abidjan, Ivory Coast.
[Ti] Title:A rare case of important and recurrent abnormal uterine bleeding in a post partum woman caused by cavernous hemangioma: a case report and review of literature.
[So] Source:Pan Afr Med J;28:130, 2017.
[Is] ISSN:1937-8688
[Cp] Country of publication:Uganda
[La] Language:eng
[Ab] Abstract:The cavernous hemangioma is a rare benign vascular tumor. About 50 cases of this disease were found in the literature over the last century and only 9 cases of cavernous hemangioma on the pregnant uterus were published it comes into cavernous or capillary form. The symptomatology is not unequivocal and when it occurs during pregnancy or postpartum, it causes life-threatening cataclysmic hemorrhage. Antenatal diagnosis is difficult and requires a multidisciplinary approach with pathologists, radiologists and gynecologists to avoid these complications or unnecessary hysterectomies. The diagnosis is histological. Hysterectomy is possible after failure of conservative treatment means. We report a rare case, a novel mixed cavernous hemangioma of the body associated with a capillary hemangioma of the cervix in a patient of 28 years 5th visors with recurrent genital bleeding in the postpartum period leading to a hysterectomy.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Process
[do] DOI:10.11604/pamj.2017.28.130.10084

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[PMID]: 29515105
[Au] Autor:Rani B; Malfettone A; Dituri F; Soukupova J; Lupo L; Mancarella S; Fabregat I; Giannelli G
[Ad] Address:School of Medicine, University of Bari, Bari, Italy.
[Ti] Title:Galunisertib suppresses the staminal phenotype in hepatocellular carcinoma by modulating CD44 expression.
[So] Source:Cell Death Dis;9(3):373, 2018 Mar 07.
[Is] ISSN:2041-4889
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Cancer stem cells (CSCs) niche in the tumor microenvironment is responsible for cancer recurrence and therapy failure. To better understand its molecular and biological involvement in hepatocellular carcinoma (HCC) progression, one can design more effective therapies and tailored then to individual patients. While sorafenib is currently the only approved drug for first-line treatment of advanced stage HCC, its role in modulating the CSC niche is estimated to be small. By contrast, transforming growth factor (TGF)-ß pathway seems to influence the CSC and thus may impact hallmarks of HCC, such as liver fibrosis, cirrhosis, and tumor progression. Therefore, blocking this pathway may offer an appealing and druggable target. In our study, we have used galunisertib (LY2157299), a selective ATP-mimetic inhibitor of TGF-ß receptor I (TGFßI/ALK5) activation, currently under clinical investigation in HCC patients. Because the drug resistance is mainly mediated by CSCs, we tested the effects of galunisertib on stemness phenotype in HCC cells to determine whether TGF-ß signaling modulates CSC niche and drug resistance. Galunisertib modulated the expression of stemness-related genes only in the invasive (HLE and HLF) HCC cells inducing a decreased expression of CD44 and THY1. Furthermore, galunisertib also reduced the stemness-related functions of invasive HCC cells decreasing the formation of colonies, liver spheroids and invasive growth ability. Interestingly, CD44 loss of function mimicked the galunisertib effects on HCC stemness-related functions. Galunisertib treatment also reduced the expression of stemness-related genes in ex vivo human HCC specimens. Our observations are the first evidence that galunisertib effectiveness overcomes stemness-derived aggressiveness via decreased expression CD44 and THY1.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review
[do] DOI:10.1038/s41419-018-0384-5

  7 / 396355 MEDLINE  
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[PMID]: 29511676
[Au] Autor:Rai N; Veeroju S; Schymura Y; Janssen W; Wietelmann A; Kojonazarov B; Weissmann N; Stasch JP; Ghofrani HA; Seeger W; Schermuly RT; Novoyatleva T
[Ad] Address:Universities of Giessen and Marburg Lung Centre (UGMLC), Aulweg 130, 35392 Giessen, Germany.
[Ti] Title:Effect of Riociguat and Sildenafil on Right Heart Remodeling and Function in Pressure Overload Induced Model of Pulmonary Arterial Banding.
[So] Source:Biomed Res Int;2018:3293584, 2018.
[Is] ISSN:2314-6141
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Pulmonary arterial hypertension (PAH) is a progressive disorder characterized by remodeling of the pulmonary vasculature and a rise in right ventricular (RV) afterload. The increased RV afterload leads to right ventricular failure (RVF) which is the reason for the high morbidity and mortality in PAH patients. The objective was to evaluate the therapeutic efficacy and antiremodeling potential of the phosphodiesterase type 5 (PDE5) inhibitor sildenafil and the soluble guanylate cyclase stimulator riociguat in a model of pressure overload RV hypertrophy induced by pulmonary artery banding (PAB). Mice subjected to PAB, one week after surgery, were treated with either sildenafil (100 mg/kg/d, = 5), riociguat (30 mg/kg/d, = 5), or vehicle ( = 5) for 14 days. RV function and remodeling were assessed by right heart catheterization, magnetic resonance imaging (MRI), and histomorphometry. Both sildenafil and riociguat prevented the deterioration of RV function, as determined by a decrease in RV dilation and restoration of the RV ejection fraction (EF). Although both compounds did not decrease right heart mass and cellular hypertrophy, riociguat prevented RV fibrosis induced by PAB. Both compounds diminished TGF-beta1 induced collagen synthesis of RV cardiac fibroblasts . Treatment with either riociguat or sildenafil prevented the progression of pressure overload-induced RVF, representing a novel therapeutic approach.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Process
[do] DOI:10.1155/2018/3293584

  8 / 396355 MEDLINE  
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[PMID]: 29508455
[Au] Autor:Palma JA; Kaufmann H
[Ad] Address:Department of Neurology, Dysautonomia Center, New York University School of Medicine, New York, New York, USA.
[Ti] Title:Treatment of autonomic dysfunction in Parkinson disease and other synucleinopathies.
[So] Source:Mov Disord;33(3):372-390, 2018 Mar.
[Is] ISSN:1531-8257
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Dysfunction of the autonomic nervous system afflicts most patients with Parkinson disease and other synucleinopathies such as dementia with Lewy bodies, multiple system atrophy, and pure autonomic failure, reducing quality of life and increasing mortality. For example, gastrointestinal dysfunction can lead to impaired drug pharmacodynamics causing a worsening in motor symptoms, and neurogenic orthostatic hypotension can cause syncope, falls, and fractures. When recognized, autonomic problems can be treated, sometimes successfully. Discontinuation of potentially causative/aggravating drugs, patient education, and nonpharmacological approaches are useful and should be tried first. Pathophysiology-based pharmacological treatments that have shown efficacy in controlled trials of patients with synucleinopathies have been approved in many countries and are key to an effective management. Here, we review the treatment of autonomic dysfunction in patients with Parkinson disease and other synucleinopathies, summarize the nonpharmacological and current pharmacological therapeutic strategies including recently approved drugs, and provide practical advice and management algorithms for clinicians, with focus on neurogenic orthostatic hypotension, supine hypertension, dysphagia, sialorrhea, gastroparesis, constipation, neurogenic overactive bladder, underactive bladder, and sexual dysfunction. © 2018 International Parkinson and Movement Disorder Society.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review
[do] DOI:10.1002/mds.27344

  9 / 396355 MEDLINE  
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[PMID]: 29509593
[Au] Autor:Iarrobino NA; Gill B; Bernard ME; Mishra MV; Champ CE
[Ad] Address:University of Pittsburgh School of Medicine.
[Ti] Title:Targeting Tumor Metabolism With Statins During Treatment for Advanced-stage Pancreatic Cancer.
[So] Source:Am J Clin Oncol;, 2018 Mar 05.
[Is] ISSN:1537-453X
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:INTRODUCTION: A growing body of preclinical data suggests that statins may exert potent antitumor effects, yet the interactions of these medications with standard therapies and clinical outcomes in this population is less clear. We assessed the impact of statin use on outcomes in patients with advanced-stage pancreatic adenocarcinoma undergoing various treatments. MATERIALS AND METHODS: After institutional review board approval, we conducted a retrospective-cohort study consisting of 303 newly diagnosed advanced-stage pancreatic adenocarcinoma patients to determine the impact of statin use on outcomes. Univariate and multivariable Cox proportional hazard regression models were utilized to estimate hazard ratios (HRs). Time-to-event was estimated using Kaplan-Meier survival analysis for overall survival, distant metastasis, and locoregional failure. Baseline and active statin usage were assessed and to mitigate risk of immortal time bias, subanalysis excluding patients with under 6 months of follow-up was conducted. RESULTS: Both prior (P=0.021) and active (P=0.030) statin usage correlated with improved survival in this cohort. Surgery, chemoradiation, and statin use improved 2-year survival rates (84.1% vs. 55.0%; P<0.001). On multivariable analysis, statin exposure was associated with overall survival (HR, 0.662; P=0.027) and trended to significance for freedom from distant metastasis (HR, 0.577; P=0.060). Comorbid conditions were not significantly associated with outcomes. CONCLUSIONS: Statin use was associated with improved overall survival in advanced-stage pancreatic adenocarcinoma patients. This data supports previous findings in early-stage pancreatic adenocarcinoma and other cancer sites. To our knowledge this is the first report to examine the efficacy of statin use as a supplementary treatment option in advanced-stage pancreatic adenocarcinoma patients.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:Publisher
[do] DOI:10.1097/COC.0000000000000433

  10 / 396355 MEDLINE  
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[PMID]: 29506558
[Au] Autor:Habuka M; Wada Y; Kurosawa Y; Yamamoto S; Tani Y; Ohashi R; Ajioka Y; Nakano M; Narita I
[Ad] Address:Division of Clinical Nephrology and Rheumatology, Niigata University Graduate School of Medical and Dental Sciences, 1-757 Asahimachi-dori, Chuo-ku, Niigata City, Niigata, 951-8510, Japan.
[Ti] Title:Fatal visceral disseminated varicella zoster infection during initial remission induction therapy in a patient with lupus nephritis and rheumatoid arthritis-possible association with mycophenolate mofetil and high-dose glucocorticoid therapy: a case report.
[So] Source:BMC Res Notes;11(1):165, 2018 Mar 05.
[Is] ISSN:1756-0500
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: Visceral disseminated varicella zoster viral (VZV) infection is a rare but severe complication with a high mortality rate in immunosuppressed individuals, and an increased susceptibility to VZV has been reported in kidney transplant recipients who are treated with mycophenolate mofetil (MMF). In Japan, MMF is currently approved for patients with lupus nephritis (LN) and data to indicate its optimal dosage are still insufficient. CASE PRESENTATION: A 46-year-old Japanese woman with rheumatoid arthritis was diagnosed as having systemic lupus erythematosus (SLE) and LN class III (A/C). Although initial remission-induction therapy with prednisolone and tacrolimus was started, her serum creatinine level and urinary protein excretion were elevated. Methylprednisolone pulse therapy was added, and tacrolimus was switched to MMF. Two months after admission when she was taking 40 mg of PSL and 1500 mg of MMF daily, she suddenly developed upper abdominal pain and multiple skin blisters, and disseminated visceral VZV infection was diagnosed. Laboratory examinations demonstrated rapid exacerbation of severe acute liver failure and coagulation abnormalities despite immediate multidisciplinary treatment, and she died of hemorrhagic shock 7 days after the onset of abdominal pain. A serum sample collected at the time of admission revealed that she had recursive VZV infection. CONCLUSIONS: MMF together with high-dose glucocorticoid therapy may increase the risk of VZV infection in Asian patients with SLE. Accumulation of evidence for parameters of safety, such as the area under the blood concentration-time curve of mycophenolic acid, should be urgently considered in order to establish a safer protocol for remission induction therapy in Asian patients with LN.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Process
[do] DOI:10.1186/s13104-018-3271-3


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