tbuckley/cabot-search huggingface dataset:
Management of Hepatocellular Carcinoma in Japan as a World-Leading Model
Authors: Masatoshi Kudo
Journal: Liver Cancer (2017)

Japan has achieved highly favorable outcomes in hepatocellular carcinoma (HCC) treatment. Several factors contributed to this achievement as shown in Tables ​Tables11 and ​and2.2. The establishment of a nationwide liver cancer screening program, which was developed in the 1980s and involves institutes across all over Japan, is one of such factors. For example, Japan was the first country in the world to develop and implement diagnostic ultrasound systems for liver cancer screening. In addition to the already established tumor marker α-fetoprotein (AFP), other markers such as protein induced by vitamin K absence or antagonist-II (PIVKA-II) and Lens culinaris-agglutinin-reactive fraction of AFP (AFP-L3) were developed in Japan. These two tumor markers were included among health insurance-covered screening tests in 1989 and 1994, respectively. Japan is the only country in the world in which these three tumor markers are included in routine surveillance under national health insurance without restrictions. Other important achievements in Japan include the invention of transcatheter arterial chemoembolization (TACE) [1], the development and the world's first commercialization of technetium-99m galactosyl human serum albumin liver scintigraphy for the assessment of hepatic functional reserve [2,3], the world's first hepatectomy [4], the development of anatomic liver resection [5], and the invention of local ablation (percutaneous ethanol injection) [6] and percutaneous microwave coagulation therapy [7]. Japan also has the highest number of cases treated with radiofrequency ablation (RFA). Other methods developed in Japan include contrast-enhanced liver ultrasound (initially by intra-arterial infusion of carbon dioxide microbubbles) [8,9]; fusion imaging; perfluorobutane (Sonazoid), a unique ultrasound contrast agent that enables Kupffer-phase imaging; and defect reperfusion imaging using Sonazoid, which assists in screening, definitive diagnosis, and local ablation therapy [10].

Table 1

Epoch-making developments, which were established in Japan first in the world
Myeloid Cell-Derived Reactive Oxygen Species Induce Epithelial Mutagenesis
Authors: Özge Canli, Adele M. Nicolas, Jalaj Gupta, Fabian Finkelmeier, Olga Goncharova, Marina Pesic, Tobias Neumann, David Horst, Martin Löwer, Ugur Sahin, Florian R. Greten
Journal: Cancer Cell (2017)
The macrophage phenotype and inflammasome component NLRP3 contributes to nephrocalcinosis-related chronic kidney disease independent from IL-1–mediated tissue injury
Authors: Hans-Joachim Anders, Beatriz Suarez-Alvarez, Melissa Grigorescu, Orestes Foresto-Neto, Stefanie Steiger, Jyaysi Desai, Julian A. Marschner, Mohsen Honarpisheh, Chongxu Shi, Jutta Jordan, Lisa Müller, Nicolai Burzlaff, Tobias Bäuerle, Shrikant R. Mulay
Journal: Kidney International (2017)

Primary/secondary hyperoxalurias involve nephrocalcinosis-related chronic kidney disease (CKD) leading to end-stage kidney disease. Mechanistically, intrarenal calcium oxalate crystal deposition is thought to elicit inflammation, tubular injury and atrophy, involving the NLRP3 inflammasome. Here, we found that mice deficient in NLRP3 and ASC adaptor protein failed to develop nephrocalcinosis, compromising conclusions on nephrocalcinosis-related CKD. In contrast, hyperoxaluric wild-type mice developed profound nephrocalcinosis. NLRP3 inhibition using the β-hydroxybutyrate precursor 1,3-butanediol protected such mice from nephrocalcinosis-related CKD. Interestingly, the IL-1 inhibitor anakinra had no such effect, suggesting IL-1-independent functions of NLRP3. NLRP3 inhibition using 1,3-butanediol treatment induced a shift of infiltrating renal macrophages from pro-inflammatory (CD45+F4/80+CD11b+CX3CR1+CD206-) and pro-fibrotic (CD45+F4/80+CD11b+CX3CR1+CD206+TGFβ+) to an anti-inflammatory (CD45+F4/80+CD11b+CD206+TGFβ-) phenotype, and prevented renal fibrosis. Finally, in vitro studies with primary murine fibroblasts confirmed the non-redundant role of NLRP3 in the TGF-β signaling pathway for fibroblast activation and proliferation independent of the NLRP3 inflammasome complex formation. Thus, nephrocalcinosis-related CKD involves NLRP3 but not necessarily via intrarenal IL-1 release but rather via other biological functions including TGFR signaling and macrophage polarization. Hence, NLRP3 may be a promising therapeutic target in hyperoxaluria and nephrocalcinosis.
The periodontal pocket: pathogenesis, histopathology and consequences
Authors: Dieter D. Bosshardt
Journal: Periodontology 2000 (2017)

The conversion of junctional epithelium to pocket epithelium is regarded as a hallmark in the development of periodontitis. Knowledge of factors contributing to the initiation and progression of pocket formation is important and may result in the development of better preventive measures and improve healing outcomes after therapeutic interventions. The periodontal pocket is a pathologically deepened gingival sulcus. In healthy periodontal conditions, the defense mechanisms are generally sufficient to control the constant microbiological challenge through a normally functioning junctional epithelium and the concentrated powerful mass of inflammatory and immune cells and macromolecules transmigrating through this epithelium. In contrast, destruction of the structural integrity of the junctional epithelium, which includes disruption of cell-to-cell contacts and detachment from the tooth surface, consequently leading to pocket formation, disequilibrates this delicate defense system. Deepening of the pocket apically, and also horizontal expansion of the biofilm on the tooth root, puts this system to a grueling test. There is no more this powerful concentration of defense cells and macromolecules that are discharged at the sulcus bottom and that face a relatively small biofilm surface in the gingival sulcus. In a pocket situation, the defense cells and the macromolecules are directly discharged into the periodontal pocket and the majority of epithelial cells directly face the biofilm. The thinning of the epithelium and its ulceration increase the chance for invasion of microorganisms and their products into the soft connective tissue and this aggravates the situation. Depending on the severity and duration of disease, a vicious circle may develop in the pocket environment, which is difficult or impossible to break without therapeutic intervention.
Reply to: Comment on “Association of bullous pemphigoid with malignancy: A systematic review and meta-analysis”
Authors: Lihi Atzmony, Ilit Mimouni, Ofer Reiter, Yael Anne Leshem, Omar Taha, Michael Gdalevich, Emmilia Hodak, Daniel Mimouni
Journal: Journal of the American Academy of Dermatology (2017)
Abstract 17882: GlycA, a Novel Inflammatory Marker, Is Strongly Associated With Mortality in Both Women and Men
Authors: Bethany Doran, Carol Haynes, Robert McGarrah, William E Kraus, Damian Craig, Svati H Shah
Journal: Circulation (2016)

Introduction:  GlycA is a novel inflammatory marker highly associated with cardiovascular (CV) morbidity and mortality. Hs-CRP is known to have a strong association with mortality in men, but not women; whether the association between GlycA with mortality differs by sex is not known.   Methods:  GlycA was measured using NMR spectroscopy in the CATHGEN biorepository linked to mortality data (n=8,436). The proportional hazards assumption was violated in cox hazards modeling; thus flexible parametric modeling was used. Interaction between sex and GlycA in full model adjusted for age, race, history of DM, HTN, obesity, smoking, and prior MI was significant (p    Results:  Over a mean of 6.6 years, 28.2% women and 30.9% men died. Women had greater median GlycA plasma concentrations at baseline (387.4 vs. 357.3 μmol/L; women vs. men). Compared to the lowest quartile of GlycA, those in the highest quartile of GlycA had a strong association with mortality in both sexes; hazard ratio 2.24 (p   Conclusions:  GlycA has a strong, graded association with mortality by increasing quartile of GlycA in both men and women; this is in contrast to hs-CRP. More research is needed as to whether GlycA may be a more reliable measure of inflammation in women.
Brote de infección por Salmonella dublin en Francia, noviembre - diciembre 1.995
Authors: V Vaillant, S Haeghebaert, J C Desenclos, P Bouvet, F Grimont, P. A.D. Grimont, A P Burnens
Journal: Eurosurveillance (1996)

El 20 de diciembre de 1.995, la Red Nacional de Salud Publica (Reseau National de Sante Publique - RNSP) recibio notificacion del Centro Nacional de Referencia de Salmonella y Shigella (Centre National de Reference - CNR) sobre un numero mayor de lo previsto de aislamientos de Salmonella dublin en personas, en noviembre y diciembre de 1.995. Gracias a la red de vigilancia europea Salm-Net, el RNSP ya conocia el brote de infeccion por S. dublin que habia tenido lugar en Suiza en el mes de noviembre. Esta epidemia fue atribuida al consumo de queso elaborado con leche cruda de vaca en la region francesa de Doubs. La correlacion entre los dos datos sugeria que este queso podria estar relacionado con el brote frances.
PS01.06: Tumor Heterogeneity in Lesion Specific Response Creates ROS1 Fusion Mediating Resistance to Gefitinib in EGFR 19 Deletion Lung Adenocarcinoma
Authors: Xiaomin Niu, Xinghao Ai, Zhiwei Chen, Shaochuan Chuai, Yi Yang, Shun Lu
Journal: Journal of Thoracic Oncology (2016)
Effect of population viral load on prospective HIV incidence in a hyperendemic rural African community
Authors: Frank Tanser, Alain Vandormael, Diego Cuadros, Andrew N. Phillips, Tulio de Oliveira, Andrew Tomita, Till Bärnighausen, Deenan Pillay
Journal: Science Translational Medicine (2017)

We propose HIV population viral load indices, which we demonstrate predict future risk of acquiring HIV in a rural South African population.
Abstract 17523: Improved Rates of Bystander Cardiopulmonary Resuscitation and Survival Consistent Across Socioeconomic Spectrum: Results From the North Carolina HeartRescue Project
Authors: Carolina Malta Hansen, Kristian Kragholm, David A Pearson, Clark Tyson, Matthew E Dupre, James G Jollis, Benjamin Strauss, Monique L Anderson, Christopher B Fordyce, Bryan McNally, Terry VandenHoek, Christopher B Granger
Journal: Circulation (2015)

Introduction: Data have shown that out of hospital cardiac arrest (OHCA) patients in lower socioeconomic status (SES) groups have lower rates of bystander intervention and survival. Following the North Carolina HeartRescue project, we explored whether improved rates of statewide bystander cardiopulmonary resuscitation (CPR) and survival are consistent across SES. Hypothesis: Statewide efforts have improved both bystander CPR and survival following OHCA irrespective of SES. Methods: Using the CARES registry, we identified and geocoded OHCAs from counties with complete case capture from 2010-14 in North Carolina (population 3 million). We divided patients (n=7,220) into tertiles of census-determined neighborhood SES by % with high school degree and median household income. Results: Rates of bystander CPR improved significantly irrespective of neighborhood SES level as determined by % with a high school degree or median household income, but remained highest for those with highest SES (Figure). The increase in survival rates significantly differed between SES groups (interaction p&lt;0.05), and the greatest increase was in the lowest tertile: 144% increase for lowest % of high school degree and 66% increase for lowest median household income. The absolute difference in survival between the highest and the lowest tertile decreased from 3.3% in 2010 to 1.8% in 2014 according to % with a high school degree, p for trend 0.001; and from 2.1% to 0.9% according to median household income, p=0.002. Conclusion: Following 4 years of the HeartRescue quality improvement program, there were substantial improvements in bystander CPR and survival, which was consistent across socioeconomic status. The greatest increase in survival appeared to be among lower SES. The absolute differences in rates of bystander CPR and survival between the highest and lowest tertiles for neighborhood level of high school degree and median household income appear to have narrowed during this period.
Increased postprandial glucagon-like peptide-1 (GLP-1) production after endoscopic gastrointestinal bypass using the Cousin lumen-apposing stent in a porcine model
Authors: Robert Caiazzo, Julien Branche, Mehdi Daoudi, Gilles Solecki, Thomas Hubert, Audrey Quenon, Violeta Raverdy, François Cousin, François Henin, Valery Dalle, Stéphane Noel, Geoffroy Vanbiervliet, Marc Barthet, François Pattou
Journal: Endoscopy (2017)

Abstract Background and study aims Endoscopic techniques have demonstrated their effectiveness in metabolic surgery, notably through a gastrointestinal (GI) liner, with a less invasive approach than conventional surgery. Our study evaluates the safety and efficacy of endoscopic GI anastomosis (EGIA) using a lumen-apposing stent to secure the anastomosis. Materials and methods EGIA was performed using the transgastric approach with a two-channel endoscope with a novel stent (Cousin Biotech). First, a safety study with a follow-up of 12 months was performed on five piglets. Then, metabolic changes were investigated in a minipig model (n = 10) before and after EGIA or open GIA (OGIA). Results EGIA was technically successful with no complications observed during clinical monitoring. Endoscopic and postmortem examinations during the second part of study showed a secure anastomosis between the stomach and the intestinal limb in all except one minipig. Both minipigs subjected to EGIA and those in the control group (OGIA) exhibited increased postprandial glucagon-like peptide-1 (GLP-1) production (incretin secretion) and impaired D-xylose absorption (malabsorption effect). Conclusion Performing EGIA with this dedicated stent appears safe, technically feasible, durable, and reproducible in providing a simple and effective endoscopic GI bypass capable of ensuring metabolic effect.
The deubiquitinating enzyme TNFAIP3 mediates inactivation of hepatic ASK1 and ameliorates nonalcoholic steatohepatitis
Authors: Peng Zhang, Pi-Xiao Wang, Ling-Ping Zhao, Xin Zhang, Yan-Xiao Ji, Xiao-Jing Zhang, Chun Fang, Yue-Xin Lu, Xia Yang, Mao-Mao Gao, Yan Zhang, Song Tian, Xue-Yong Zhu, Jun Gong, Xin-Liang Ma, Feng Li, Zhihua Wang, Zan Huang, Zhi-Gang She, Hongliang Li
Journal: Nature Medicine (2017)
T-lymphoblastic lymphomas expressing the non-disulfide-linked form of the T-cell receptor gamma/delta: characterization with monoclonal antibodies and genotypic analysis
Authors: B Falini, L Flenghi, M Fagioli, MF Martelli, S Pileri, F Grignani, A Beltrami, D Novero, PG Pelicci
Journal: Blood (1989)
Abstract 15008: Bone Marrow Plasma Fibroblast Growth Factor 23 Levels Are a Strong Predictor of Death in Patients With Chronic Heart Failure
Authors: Beatrice von Jeinsen, Kateryna Sopova, Lars Palapies, Stephan Fichtlscherer, Florian Seeger, Stefanie Dimmeler, Birgit Assmus, Andreas M Zeiher, Till Keller
Journal: Circulation (2016)

Introduction and Aim:  Fibroblast growth factor 23 (FGF-23) is primarily known as a regulator in phosphate and calcium homeostasis. It has been described that FGF-23 might play a role in cardiovascular disease: peripheral FGF-23 levels are associated with left ventricular hypertrophy, coronary artery disease and chronic heart failure (CHF). Aim of the present study was to evaluate the prognostic information of FGF-23 measured in bone marrow plasma (FGF BM -23) as well as in peripheral blood samples (FGF PB -23) of patients with CHF.   Methods:  In 237 patients (age 61.4±12.2) with CHF, who were enrolled in the Frankfurt Bone Marrow-Derived Cell Therapy Registry, and in 49 healthy control individuals (age 39.1±10.8), FGF PB -23 and FGF BM -23 levels were measured. Within a 5-year-follow up period, out of the 237 patients with CHF, 54 patients (23%) died, used as outcome measure.   Results:  Both, FGF BM -23 and FGF PB -23 were significantly increased in CHF patients compared to healthy individuals (p BM -23 levels were higher than FGF PB -23 levels. Furthermore, in patients who died within 5 years, FGF BM -23 as well as FGF PB -23 was increased compared to survivors (p BM -23 as well as FGF PB -23 at baseline did correlate with ejection fraction (EF), estimated glomerular filtration rate (eGFR) and age (all p PB -23 and FGF BM -23 were strongly associated with death with hazard ration (HR) of 1.41 (1.214, 1.638; p PB -23 and FGF BM -23 remained significant independent indicators for death with HR of 1.352 (1.14, 1.603; p   Conclusion:  In patients with chronic heart failure, elevated FGF-23 measured in bone marrow plasma and in peripheral blood is strongly associated with long-term mortality. These findings underline the importance of the heart-bone axis in heart failure development and Progression.
Abstract 17000: Activation of Igf-1 Receptor Signaling by Hyperinsulinemia Suppresses Cardiac Autophagy Through Trb3/p62 Pathway
Authors: Karla Maria Pires, Olesya Ilkun, Maricio Augusto Buffolo, Shaobo Pei, Evan Dale Abel, Sihem Boudina
Journal: Circulation (2016)

Introduction:  Insulin and insulin-like growth factor (IGF) receptor signaling is a known suppressor of autophagy in the heart. Therefore, one would predict to see higher levels of autophagy in the insulin resistant heart but the opposite is reported in the literature.   Hypothesis:  Thus, the aim of this study was to investigate the mechanisms involved in autophagy-suppression in insulin resistant hearts.   Methods:  We assessed autophagic flux in the hearts of mouse models with either impaired insulin signaling and cardiac insulin resistance ( ob/ob  mice) or absent insulin signaling specifically in cardiomyocytes (CIRKO mice) or in the entire heart (TIRKO mice).   Results:  Autophagic flux was impaired in the hearts of ( ob/ob ) and TIRKO mice but not in hearts of CIRKO mice. One common characteristic of ( ob/ob ) and TIRKO mice is that they both exhibit systemic hyperinsulinemia and they both have increased IGF-1 receptor signaling in the heart. Thus, we hypothesized that systemic hyperinsulinema activates IGF-1 receptor signaling to suppress cardiac autophagy. To directly test that, we generated ( ob/ob ) and TIRKO mice lacking one allele of the IGF-1 receptor in cardiomyocytes and showed that autophagy was restored in these hearts. Furthermore, reduction of IGF-1 receptor signaling in TIRKO hearts reduced p62 accumulation and diminished TRB3 expression.   Conclusion:  Taken together, these results demonstrated for the first time that systemic hyperinsulinemia suppresses cardiac autophagy through IGF-1 receptor signaling to TRB3/p62.
Infezioni gastro-intestinali tra i turisti: di chi la responsabilità?
Authors: R Cartwright
Journal: Eurosurveillance (2004)

I progressi nella sanita pubblica e nel controllo delle malattie trasmissibili in Europa sono stati possibili non soltanto grazie agli sforzi dei medici di sanita pubblica ma anche grazie a un approccio multidisciplinare. I risultati dell'equipe spagnola che ha investigato sull'epidemia di gastroenterite tra i turisti nella Repubblica Domenicana sono un buon esempio della necessita di una cooperazione tra discipline e tra paesi. A livello mondiale il turismo e tra le tre forze economiche piu importanti, il numero dei turisti non cessando di crescere ogni anno. Si stima in piu di 70 milioni l'anno il numero di viaggi organizzati venduti in Europa con destinazione in tutte le parti del mondo. I turisti sono cosi esposti a una varieta di ambienti e di organismi patogeni.
Glut3 Addiction Is a Druggable Vulnerability for a Molecularly Defined Subpopulation of Glioblastoma
Authors: Érika Cosset, Sten Ilmjärv, Valérie Dutoit, Kathryn Elliott, Tami von Schalscha, Maria F. Camargo, Alexander Reiss, Toshiro Moroishi, Laetitia Seguin, German Gomez, Jung-Soon Moo, Olivier Preynat-Seauve, Karl-Heinz Krause, Hervé Chneiweiss, Jann N. Sarkaria, Kun-Liang Guan, Pierre-Yves Dietrich, Sara M. Weis, Paul S. Mischel, David A. Cheresh
Journal: Cancer Cell (2017)
A randomized phase II study evaluating different maintenance schedules of nab-paclitaxel in the first-line treatment of metastatic breast cancer: final results of the IBCSG 42-12/BIG 2-12 SNAP trial
Authors: A. Gennari, Z. Sun, U. Hasler-Strub, M. Colleoni, M.J. Kennedy, R. Von Moos, J. Cortés, M.J. Vidal, B. Hennessy, J. Walshe, K. Amillano Parraga, K. Ribi, J. Bernhard, S. Morales Murillo, O. Pagani, A. Barbeaux, S. Borstnar, M. Rabaglio-Poretti, R. Maibach, M.M. Regan, G. Jerusalem
Journal: Annals of Oncology (2017)
Abstract 17388: Applicability of a Western Model of Hypertension in a Yup'ik Eskimo Population
Authors: Eric T Roberts, Scarlett Hopkins, Bert Boyer, Bernadette Boden-Albala
Journal: Circulation (2011)

Hypertension (HT) is a powerful contributor to cardiovascular disease. Importantly, HT is becoming increasingly common in non-western and rural contexts. While much literature has clarified the role of- and risk factors for HT in urban, western contexts little is known about the relevance of these results to other populations. This abstract explores the applicability of a western model of HT to a sample of Yup'ik Eskimo people. As part of the Center for Alaskan Native Health Research study we interviewed Yup'ik individuals residing in 7 rural villages located in Southwestern Alaska. Covariates of interest were age, sex, education, body composition, physical activity, tobacco use, household composition, and ethnic identification. We assessed the association between vascular risk factors and the odds of having either normal (systolic 120 to 129 mmHg) or borderline to hypertensive (systolic ≥ 130 mmHg) as compared to optimal (systolic &lt; 120 mmHg) blood pressure with multinomial logistic regressions. Data comes from 1015 Yup'ik individuals: 54% female, mean age 37.6 (SD 17.4). Mean systolic BP was 120.07 mmHg, 20.7% had systolic BP ≥ 130 mmHg. In our final model age (one year increase; odds ratio = 1.06), male sex (1.46), waist circumference (one cm increase; 1.04), ever smoking tobacco (1.31), being single (compared to married; 1.44), and having 4 or more biological children (compared to none; 0.74) were associated with having borderline or definite hypertension. A similar pattern was observed for the presence of normal blood pressure as compared to optimal blood pressure - age (1.02), male sex (1.79), waist circumference (1.02), ever smoking tobacco (1.21), and being single (compared to married; 1.62). There were no direct effects of education, physical activity, or ethnic identification on the odds of HT. Interactions suggest individuals identifying highly with both Yup'ik and White culture have slower age related increases in HT, and that high levels of education negate differences in HT across all categories of ethnic identification. HT is emerging as an important risk factor among Yup'ik and other Alaskan Native people. Western models for HT may be applicable to Alaska Native populations; differences may elucidate causes and mechanisms across populations.