tbuckley/cabot-search huggingface dataset:
Understanding the gut–kidney axis in nephrolithiasis: an analysis of the gut microbiota composition and functionality of stone formers
Authors: Andrea Ticinesi, Christian Milani, Angela Guerra, Franca Allegri, Fulvio Lauretani, Antonio Nouvenne, Leonardo Mancabelli, Gabriele Andrea Lugli, Francesca Turroni, Sabrina Duranti, Marta Mangifesta, Alice Viappiani, Chiara Ferrario, Rossella Dodi, Margherita Dall’Asta, Daniele Del Rio, Marco Ventura, Tiziana Meschi
Journal: Gut (2018)

Objectives The involvement of the gut microbiota in the pathogenesis of calcium nephrolithiasis has been hypothesised since the discovery of the oxalate-degrading activity of Oxalobacter formigenes , but never comprehensively studied with metagenomics. The aim of this case–control study was to compare the faecal microbiota composition and functionality between recurrent idiopathic calcium stone formers (SFs) and controls. Design Faecal samples were collected from 52 SFs and 48 controls (mean age 48±11). The microbiota composition was analysed through 16S rRNA microbial profiling approach. Ten samples (five SFs, five controls) were also analysed with deep shotgun metagenomics sequencing, with focus on oxalate-degrading microbial metabolic pathways. Dietary habits, assessed through a food-frequency questionnaire, and 24-hour urinary excretion of prolithogenic and antilithogenic factors, including calcium and oxalate, were compared between SFs and controls, and considered as covariates in the comparison of microbiota profiles. Results SFs exhibited lower faecal microbial diversity than controls (Chao1 index 1460±363vs 1658±297, fully adjusted p=0.02 with stepwise backward regression analysis). At multivariate analyses, three taxa ( Faecalibacterium , Enterobacter , Dorea ) were significantly less represented in faecal samples of SFs. The Oxalobacter abundance was not different between groups. Faecal samples from SFs exhibited a significantly lower bacterial representation of genes involved in oxalate degradation, with inverse correlation with 24-hour oxalate excretion (r=−0.87, p=0.002). The oxalate-degrading genes were represented in several bacterial species, whose cumulative abundance was inversely correlated with oxaluria (r=−0.85, p=0.02). Conclusions Idiopathic calcium SFs exhibited altered gut microbiota composition and functionality that could contribute to nephrolithiasis physiopathology.
Two Different Causes of Decreased Activity on Ipsilateral Iliac Artery in Renal Transplant Scintigraphy
Authors: Bulent Yazici, Aylin Oral, Mumtaz Yilmaz, Aysegül Akgün, Huseyin Toz
Journal: Clinical Nuclear Medicine (2018)

In 2 patients, perfusion images of renal transplant scintigraphy showed similarly decreased activity on ipsilateral iliac artery. One's graft was photopenic because of arterial thrombosis. However, the other's graft had sufficient perfusion and no abnormality in iliac arteries, but he had femoral arteriovenous graft for hemodialysis on the contralateral side. So, in this patient, decreased activity on ipsilateral iliac artery was probably related to increased arterial flow of the contralateral side. It should be considered that decreased activity on ipsilateral iliac artery in perfusion images is not only due to ipsilateral problem; the cause could be on the contralateral side.
Insulin Access and Affordability Working Group: Conclusions and Recommendations
Authors: William T. Cefalu, Daniel E. Dawes, Gina Gavlak, Dana Goldman, William H. Herman, Karen Van Nuys, Alvin C. Powers, Simeon I. Taylor, Alan L. Yatvin
Journal: Diabetes Care (2018)

There are more than 30 million Americans with diabetes, a disease that costs the U.S. more than $327 billion per year (1,2). Achieving glycemic control and controlling cardiovascular risk factors have been conclusively shown to reduce diabetes complications, comorbidities, and mortality. To achieve these desired outcomes, the medical community now has available many classes of medications and many formulations of insulin to effectively manage the metabolic abnormalities for people with diabetes. However, the affordability of medications in general, and for insulin specifically, is currently of great concern to people with diabetes, their families, health care providers, insurers, and employers. For millions of people living with diabetes, including all individuals with type 1 diabetes, access to insulin is literally a matter of life and death. The average list price of insulin has skyrocketed in recent years, nearly tripling between 2002 and 2013 (3). The reasons for this increase are not entirely clear but are due in part to the complexity of drug pricing in general and of insulin pricing in particular.

As the price of insulin continues to rise, individuals with diabetes are often forced to choose between purchasing their medications or paying for other necessities, exposing them to serious short- and long-term health consequences (4–9). To find solutions to the issue of insulin affordability, there must be a better understanding of the transactions throughout the insulin supply chain, the impact each stakeholder has on what people with diabetes pay for insulin, and the relative efficacy of therapeutic options. Thus, as the nation’s leading voluntary health organization whose mission is “to prevent and cure diabetes and to improve the lives of all people affected by diabetes,” the American Diabetes Association (ADA) is committed to finding ways to provide relief for individuals and families who lack affordable access …
Abstract 12609: Impaired Mitochondrial Respiration Precedes Clinical Heart Failure in Right Ventricular Pressure Overload
Authors: Nefthi Sandeep, Mingming Zhao, Donq-Qing Hu, Michael Coronado, Kristina B Kooiker, Giovanni Fajardo, Daniel Bernstein, Sushma Reddy
Journal: Circulation (2016)

Introduction: Congenital heart disease patients with right-sided obstruction have increased stress on the right ventricle (RV) leading to right ventricular hypertrophy (RVH) and failure (RVF). The critical role of mitochondrial energetics in the development of RVH and RVF is not known. We hypothesize that mitochondrial dysfunction contributes to the chronic energy deficit and mechanical dysfunction in heart failure. Methods: Adult, male FVB mice underwent pulmonary artery banding (PAB) to induce RVH (n=9) and RVF (n=4) and were compared to sham-operated controls (n=9). We used a high-resolution Oxygraph2K respirometer to measure oxygen consumption in tissue and in isolated mitochondria from the RV free wall. We evaluated leak respiration during substrate utilization by complex 1-NADH dehydrogenase and complex 2-succinate dehydrogenase and during maximal ATP generation by complex 5-ATP synthase. Groups were compared using ANOVA. Data is presented as mean ± SEM (*p&lt;0.05). Results: All mice had a PAB gradient of 30-40 mmHg by echocardiography. RVH mice had preserved systolic function while RVF mice had heart failure (ascites, tachypnea, hepatomegaly) and decreased function (Table). RVH showed preserved complex 1 mediated respiration but lower complex 2 and 5 respiration and lower respiratory control ratios (RCR) while in RVF, all complexes showed impaired respiration (Table). However, isolated mitochondria from RVF demonstrated preserved respiratory capacity when supplied with exogenous substrates and no change in complex levels. Conclusion: Mitochondrial respiration is impaired even in stable RVH and progressively worsens in RVF in vivo. Interestingly, isolated mitochondria show normal respiration in RVF when supplied with substrates ex vivo suggesting a defect with substrate delivery rather than intrinsic mitochondrial function. Strategies to enhance substrate delivery may improve ATP generation and thereby preserve function in heart failure.
Cardiotoxicity of 5‐fluorouracil and capecitabine in Chinese patients: a prospective study
Authors: Jianjun Peng, Chao Dong, Chang Wang, Weihua Li, Hao Yu, Min Zhang, Qun Zhao, Bo Zhu, Jun Zhang, Wenliang Li, Fenghua Wang, Qiong Wu, Wenhao Zhou, Ying Yuan, Meng Qiu, Gong Chen
Journal: Cancer Communications (2018)

Abstract Background 5‐Fluorouracil (5‐FU) and capecitabine‐associated cardiotoxicity ranging from asymptomatic electrocardiography (ECG) abnormalities to severe myocardial infarction has been reported in a number of studies, but such cardiotoxicity in Chinese patients with malignant diseases has not been investigated to date. In the present study, we aimed to prospectively evaluate the incidence rates and clinical manifestations of 5‐FU‐ and capecitabine‐associated cardiotoxicity in cancer patients recruited from multiple centers in China. Methods Among the 527 patients who completed the study, 196 received 5‐FU‐based chemotherapy and 331 received capecitabine‐based chemotherapy as either first‐line or adjuvant therapy. Adverse events were reported during the treatment and up to 28 days of follow‐up. Outcome measures included ECG, myocardial enzymes, cardiac troponin, brain natriuretic peptide and echocardiography. Univariate analysis and logistic regression were performed for subgroup analysis and identification of significant independent variables that are associated with cardiotoxicity of both agents. Results In total, 161 of 527 patients (30.6%) experienced cardiotoxicity. The incidence rate of cardiotoxicity was 33.8% (112/331) in the capecitabine group, which was significantly higher than the rate of 25% (49/196) in the 5‐FU group ( P = 0.0042). 110/527 patients (20.9%) suffered arrhythmia, 105/527 (19.9%) developed ischemic changes, while only 20/527 patients (3.8%) presented heart failure and 6/527 patients (1.1%) had myocardial infarction. Pre‐existing cardiac disease, hypertension, capecitabine‐based chemotherapy and duration of treatment were identified as significant risk factors associated with cardiotoxicity. The odds ratio were 15.7 (prior history of cardiac disease versus no history), 1.86 (capecitabine versus 5‐FU), 1.06 (5–8 versus 1–4 chemotherapy cycles) and 1.58 (hypertension versus no hypertension), respectively. Conclusions Cardiotoxicity induced by fluoropyrimidines in the Chinese population may be underestimated in clinical practice. Close monitoring of patients is recommended, especially for those patients at high risk for cardiotoxicity. Possible risk factors are duration of treatment, capecitabine‐based chemotherapy, pre‐existing cardiac diseases and hypertension. Trial registration This study was initiated on January 22, 2014 and has been retrospectively registered with the registration number ChiCTR1800015434
Relationship between visceral fat and portal vein thrombosis in patients with liver cirrhosis
Authors: M.H. Conde, E. Llop, M. López-Gómez, C. Perelló, C. Fernández-Carrillo, J.A. Guerra, J.L.M. Porras, N.F. Puga, M. Magaz, J.L.C. Panero
Journal: Journal of Hepatology (2018)
Publisher Correction: Single-cell analysis of experience-dependent transcriptomic states in the mouse visual cortex
Authors: Sinisa Hrvatin, Daniel R. Hochbaum, M. Aurel Nagy, Marcelo Cicconet, Keiramarie Robertson, Lucas Cheadle, Rapolas Zilionis, Alex Ratner, Rebeca Borges-Monroy, Allon M. Klein, Bernardo L. Sabatini, Michael E. Greenberg
Journal: Nature Neuroscience (2018)
TCTAP A-008 Trends of Acute Myocardial Infarction in Korea from the Experience of Korea Acute Myocardial Infarction Registry: What Is Different from Western Registries?
Authors: Yongcheol Kim, Myung-Ho Jeong, Youngkeun Ahn, Young Joon Hong, Doo Sun Sim, Min Chul Kim
Journal: Journal of the American College of Cardiology (2018)
Workplace Noise and Heart Health
Authors: Bridget Kuehn
Journal: JAMA (2018)

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Efficacy and Follow-up of Segmental or Subtotal Colectomy in Patients With Colitis-Associated Neoplasia
Authors: Noa Krugliak Cleveland, Jacob E. Ollech, Ruben J. Colman, Dylan Rodriquez, Ayal Hirsch, Russell D. Cohen, Stephen B. Hanauer, John Hart, Roger Hurst, David T. Rubin
Journal: Clinical Gastroenterology and Hepatology (2018)
Integrated biomarker analysis for 412 renal cell cancer (RCC) patients (pts) treated on the phase 3 COMPARZ trial: Correlating common mutation events in <i>PBRM1</i> and <i>BAP1</i> with angiogenesis expression signatures and outcomes on tyrosine kinase inhibitor (TKI) therapy.
Authors: Martin Henner Voss, Fengshen Kuo, David Chen, Mahtab Marker, Parul Patel, Almedina Redzematovic, Nadeem Riaz, Timothy A. Chan, Toni K. Choueiri, James Hsieh, Robert J. Motzer, A. Ari Hakimi
Journal: Journal of Clinical Oncology (2017)

4523 Background: In RCC biology mutations in PBRM1 and BAP1are largely non-overlapping and collectively affect &gt;50% of pts. How and through which mechanism they influence disease kinetics is poorly understood. Sunitinib and pazopanib inhibit angiogenesis, a key driver in RCC. We analyzed mutation status and gene expression signatures in a large cohort of pts receiving first-line sunitinib or pazopanib on the COMPARZ trial. Methods: RNA and DNA were extracted from archival tissue. PBRM1 and BAP1mutation status was determined via a custom exon-targeted platform. Transcriptome analysis was done using Affymetrix GeneChip HTA 2.0. We computed a 43 gene angiogenesis expression score with previously reported dynamic response to VEGF-directed therapy in xenograft models (Masiero, Cancer Cell 2013). DNA and RNA findings were correlated with clinical outcomes using parametric and non-parametric tests. Results: 412 pts contributed tumor RNA, 377 pts DNA; 362 pts both. PBRM1 and BAP1 were mutated (MT) in 44% and 15% of pts, respectively. Presence of PBRM1mutations correlated with superior PFS (p=0.008) and OS (p=0.004) on log-rank test, and PBRM1 mutation rate was higher in pts with objective response than those with progression (Fisher’s Exact, p=0.012). In contrast, pts with MT BAP1 had inferior OS compared to those whose were wild type (WT) (log-rank, p=0.012). Across all 412 pts angiogenesis score associated favorably with outcome on uni and multivariate analyses (Cox proportional hazard regression, OS p&lt;0.001 and PFS p&lt;0.005); scores were higher in 123 pts with objective response than 81 pts with progression as best response (Mann-Whitney, p=0.009). Angiogenesis scores were higher in PBRM1 MT vs WT patients (Mann-Whitney, p&lt;0.001), but lower in BAP1 MT vs WT patients (p&lt;0.001). Conclusions: PBRM1 and BAP1 mutations appear to have opposite effects in advanced RCC. Loss of PBRM1 enhances the pro-angiogenic microenvironment of RCC with favorable effects on response to TKI; BAP1 loss associates with decreased angiogenic signaling and adverse outcome to TKI. Clinical trial information: NCT00720941.
Significant changes of HCV patient characteristics over time in the era of direct antiviral agent therapy – are all HCV subpopulations treated similarly? – Results from the German hepatitis C Cohort
Authors: S. Christensen, P. Ingiliz, J. Schulze Zur Wiesch, K. Schewe, C. Boesecke, D. Hüppe, A. Baumgarten, L. Thomas, G. Schmutz, S.K. Georg, B. Florian, B. Heiner, S. Mauss
Journal: Journal of Hepatology (2018)
H19 Induces Abdominal Aortic Aneurysm Development and Progression
Authors: Daniel Y. Li, Albert Busch, Hong Jin, Ekaterina Chernogubova, Jaroslav Pelisek, Joakim Karlsson, Bengt Sennblad, Shengliang Liu, Shen Lao, Patrick Hofmann, Alexandra Bäcklund, Suzanne M. Eken, Joy Roy, Per Eriksson, Brian Dacken, Deepak Ramanujam, Anne Dueck, Stefan Engelhardt, Reinier A. Boon, Hans-Henning Eckstein, Joshua M. Spin, Philip S. Tsao, Lars Maegdefessel
Journal: Circulation (2018)

Background: Long noncoding RNAs have emerged as critical molecular regulators in various biological processes and diseases. Here we sought to identify and functionally characterize long noncoding RNAs as potential mediators in abdominal aortic aneurysm development. Methods: We profiled RNA transcript expression in 2 murine abdominal aortic aneurysm models, Angiotensin II (ANGII) infusion in apolipoprotein E–deficient ( ApoE −/− ) mice (n=8) and porcine pancreatic elastase instillation in C57BL/6 wild-type mice (n=12). The long noncoding RNA H19 was identified as 1 of the most highly upregulated transcripts in both mouse aneurysm models compared with sham-operated controls. This was confirmed by quantitative reverse transcription–polymerase chain reaction and in situ hybridization. Results: Experimental knock-down of H19, utilizing site-specific antisense oligonucleotides (LNA-GapmeRs) in vivo, significantly limited aneurysm growth in both models. Upregulated H19 correlated with smooth muscle cell (SMC) content and SMC apoptosis in progressing aneurysms. Importantly, a similar pattern could be observed in human abdominal aortic aneurysm tissue samples, and in a novel preclinical LDLR −/− (low-density lipoprotein receptor) Yucatan mini-pig aneurysm model. In vitro knock-down of H19 markedly decreased apoptotic rates of cultured human aortic SMCs, whereas overexpression of H19 had the opposite effect. Notably, H19-dependent apoptosis mechanisms in SMCs appeared to be independent of miR-675, which is embedded in the first exon of the H19 gene. A customized transcription factor array identified hypoxia-inducible factor 1α as the main downstream effector. Increased SMC apoptosis was associated with cytoplasmic interaction between H19 and hypoxia-inducible factor 1α and sequential p53 stabilization. Additionally, H19 induced transcription of hypoxia-inducible factor 1α via recruiting the transcription factor specificity protein 1 to the promoter region. Conclusions: The long noncoding RNA H19 is a novel regulator of SMC survival in abdominal aortic aneurysm development and progression. Inhibition of H19 expression might serve as a novel molecular therapeutic target for aortic aneurysm disease.
Considerations to facilitate a US study that replicates PREDIMED
Authors: David R. Jacobs, Kristina S. Petersen, Karianne Svendsen, Emilio Ros, Carol B. Sloan, Lyn M. Steffen, Linda C. Tapsell, Penny M. Kris-Etherton
Journal: Metabolism (2018)

The PREDIMED clinical trial provided strong evidence that a Mediterranean dietary pattern (MedDiet) could help prevent cardiovascular disease (CVD) events in high risk middle-aged/older people. This report considers the feasibility of replicating PREDIMED in the U.S., including recommendations for dietary and behavioral principles. A 14-point Mediterranean diet Adherence Score (MEDAS) guided the PREDIMED MedDiet recommendations. At baseline MEDAS points were ~8.5. During intervention this score increased to nearly 11 in MedDiet vs. 9 in control. In the MedDiet groups, only about 0.5 points of the net 2 point MEDAS increase was attributable to the gratis supplements of olive oil or nuts. An issue in a U.S. replication is the large difference in typical U.S. versus Spanish diet and lifestyle. A typical U.S. diet would achieve a MEDAS of 1-2. A replication is scientifically feasible with an assumption such as that the MedDiet reflects a continuum of specific food choices and meal patterns. As such, a 2 point change in MEDAS at any point on the continuum would be hypothesized to reduce incident CVD. A conservative approach would aim for a randomized 4 point MEDAS difference, e.g. 5-6 points vs. an average U.S. diet group that achieved only 1-2 points.
Correlation of psoriasis activity with socioeconomic status: cross-sectional analysis of patients enrolled in the Psoriasis Longitudinal Assessment and Registry (PSOLAR)
Authors: A.B. Kimball, M. Augustin, K.B. Gordon, G.G. Krueger, D. Pariser, S. Fakharzadeh, K. Goyal, S. Calabro, S. Lee, R. Lin, N. Li, B. Srivastava, L. Guenther
Journal: British Journal of Dermatology (2018)
P303Female gender-specific dysregulation of miR-29b and its target AKT-3 in experimental and clinical cardiac hypertrophy under pressure overload
Authors: R Garcia, A Gil, L Ruiz, J Gomez, M A Hurle, J F Nistal
Journal: Cardiovascular Research (2018)

development of adverse outcomes in patients with myocardial infarction seems relevant.One of the most important directions in this field is the study of biomarkers of endothelial dysfunction as predictors of adverse outcome.Purpose: the aim of the study was to evaluate the levels of biomarkers associated with endothelial dysfunction in patients after myocardial infarction (MI) depending on the outcome.Methods: 223 patients with MI at the age of 57.35610.09years was included in the study.The observation period was 18-24 months.Depending on the outcome, the patients were divided into 2 groups: 1st-55 patients (24,7%) with an adverse outcome (all-cause mortality, recurrent acute coronary syndrome, decompensate chronic heart failure); 2nd-168 patients (75,3%) with favorable outcome.We determined the levels of interleukin-6 (IL), matrix metalloproteinase-2 (MMP), highsensitivity C-reactive protein (hsCRP) by immunoenzyme method on the 3rd and 14th days in blood, circulating endothelial cells (CEC) by flow cytometry, antigen von Willebrand factor (vWF:Ag) by immunoturbidimetric method, endothelin-1 (ET-1) and superoxide dismutase (SOD) was determined by immunoenzyme method at day 14 and after 3 months MI.Statistical data are presented as the median and interquartile scale.Results: Concentrations of IL-6, MMP2 and hsSRP on day 3 were significantly higher in group 1 (14,9 [7,9;53,5] pg/ml vs 10,4[5,1;16,1] pg/ml, 29,8 [24,3;of 32.6] ng/ml vs 21,5 [18,4;24,3]ng/ml, and18.1 [10,7;40,7] mg/l vs 11,5 [6,1;28,2] mg/l, respectively (p<0.05).At day 14 the concentrations of IL-6 and hsSRP decreased and were not significantly different.Thus, elevated levels of IL-6, hsSRP and MMP-2 on day 3, are most likely related with activity of inflammatory reaction and necrosis of the myocardium.The levels of CEC and ET-1 at day 14 was increased in both groups (5[5;8]C/3[10a ˜c ¸leucocytes vs 5[1;10]C/3[10a ˜c ¸leucocytes, 0,7[0,3;1,7]fmol/ml vs 0,3[0,2;0,6]fmol/ ml, respectively, in 1st and 2nd groups) and remained increased after 3 months (6[2;10]C/3[10a ˜c ļeucocytes vs 3[2;4] C/3[10a ˜c ¸leucocytes (p¼0.048) and 1,8[0,7;3.7V] vs 0,6[0,4;1,0] (p¼0,033) in 1st and 2nd group, respectively).We have analyzed the prognostic value of biomarkers at 3, 14 days and 3 months after MI.The greatest prognostic value was determined for the high levels of IL-6 (AUC of 0.63 with 95% CI from 0.54 to 0.72), MMP-2 (AUC of 0.83 with 95% CI from 0.75 to 0.89), hsSRP (AUC of 0.65 with 95% CI from 0.54 to 0,73), ET-1 (AUC of 0.73 with 95% CI from 0.53 to 0.88) after 3 months of MI.Conclusions: High activity of inflammation, necrosis of the myocardium in the early stages of MI and persisting endothelial dysfunction associated with a poor prognosis in long term period in patients after MI.