tbuckley/cabot-search huggingface dataset:
Abstract 3047: Management Of Procedural Complications Associated With Transcatheter Aortic Valve Implantation
Authors: Ruediger Lange, Sabine Bleiziffer, Hendrik Ruge, Domenico Mazzitelli, Christian Schreiber, Andrea Hutter, Peter Tassani-Prell, Robert Bauernschmitt
Journal: Circulation (2008)

Objective The transcatheter aortic valve implantation (TAVI) technology is rapidly evolving. The complications related to these procedures are different from those seen after conventional aortic valve replacement. Herein, we report our experience on the incidence and management of procedure-related complications in the first series of TAVI. Methods Between 6/2007 and 6/2008, 112 patients (n=62 female, mean age 81.3±7y, mean logistic EuroScore 25.0±15.6%) underwent TAVI through either a retrograde (n=92 transfemoral, n=3 via subclavian artery, n=1 ascending aorta) or antegrade (n=16 transapical) approach at our institution. 95 CoreValve and 17 Edwards Sapien (n=17) prostheses were implanted. Results 30-day mortality was 8.9% (n=10). Major vascular complications occurred in 19 patients (16,9%). 2 patients with iliac or femoral rupture were treated with covered stent. 14 patients with bleeding from vascular site were treated with surgical suture or prosthesis implantation. Three patients had lethal aortic root (n=2) or abdominal (n=1) aortic rupture. Cardiac tamponade occurred in 8 patients (7.1%); among these 3 were treated conservatively, 4 underwent subxyphoid puncture and one patient had thoracotomy. Valve displacement could be treated interventionally in 5 out of 6 patients, 1 patient underwent conventional surgery. In 2 patients, with extremely poor LV function, emergent institution of cardiopulmonary bypass was required during the procedure. 5 patients underwent interventional re-valving (n=2) or surgical re-replacement (n=3) due to high-grade regurgitation (n=5) or valve displacement (n=1). Pacemaker implantation due to postprocedural AV block was required in 23 patients (20.7%). Despite these complications, the overall initial procedural success was 98 % (n= 110/112). Conclusions A significant number of complications after TAVI requires surgical treatment. Therefore, TAVI procedures should be performed in a hybrid operating room which allows for immediate surgical intervention and the rapid institution of cardiopulmonary bypass if necessary.
Seroprevalence in blood donors reveals widespread, multi-source exposure to hepatitis E virus, southern France, October 2011
Authors: J M Mansuy, K Sauné, H Rech, F Abravanel, C Mengelle, S L’Homme, F Destruel, N Kamar, J Izopet
Journal: Eurosurveillance (2015)

The apparent seroprevalence of hepatitis E Virus (HEV)varies greatly among developed countries depending on the geographical area and the sensitivity of immunoassays. We used a validated assay to determine the prevalence of HEV IgG and IgM antibodies among 3,353 blood donors living in southern France,who gave blood during the two first weeks of October 2011 and participated in the study. Demographic and epidemiological information was collected using aspecific questionnaire. We also screened 591 samples for HEV RNA. Overall IgG seroprevalence was 39.1%and varied from 20% to 71.3% depending on the geographical area (p < 0.001) while IgM seroprevalence was 3.31%. Anti-HEV IgG was significantly correlated with increasing age (p < 0.001), eating uncooked pork liver sausages (p < 0.001), offal (p = 0.003), or mussels(p = 0.02). Anti-HEV IgM was associated with being male (p = 0.01) and eating uncooked pork liver sausages(p = 0.02). HEV RNA was detected in one of the 99 anti-HEV IgM-positive samples, but in none of the 492 anti-HEV IgM-negative samples. HEV is hyperendemic in southern France. Dietary and culinary habits alone cannot explain the epidemiology of HEV in this region, indicating that other modes of contamination should be investigated.
Carcinoma-associated fibroblasts promote the stemness and chemoresistance of colorectal cancer by transferring exosomal lncRNA H19
Authors: Jing Ren, Liang Ding, Dongya Zhang, Guoping Shi, Qianyun Xu, Sunan Shen, Yaping Wang, Tingting Wang, Yayi Hou
Journal: Theranostics (2018)

Long non-coding RNAs (lncRNAs) are involved in the pathology of various tumors, including colorectal cancer (CRC). The crosstalk between carcinoma- associated fibroblasts (CAFs) and cancer cells in the tumor microenvironment promotes tumor development and confers chemoresistance. In this study, we further investigated the underlying tumor-promoting roles of CAFs and the molecular mediators involved in these processes. Methods: The AOM/DSS-induced colitis-associated cancer (CAC) mouse model was established, and RNA sequencing was performed. Small interfering RNA (siRNA) sequences were used to knock down H19. Cell apoptosis was measured by flow cytometry. SW480 cells with H19 stably knocked down were used to establish a xenograft model. The indicated protein levels in xenograft tumor tissues were confirmed by immunohistochemistry assay, and cell apoptosis was analyzed by TUNEL apoptosis assay. RNA-FISH and immunofluorescence assays were performed to assess the expression of H19 in tumor stroma and cancer nests. The AldeRed ALDH detection assay was performed to detect intracellular aldehyde dehydrogenase (ALDH) enzyme activity. Isolated exosomes were identified by transmission electron microscopy, nanoparticle tracking and Western blotting. Results: H19 was highly expressed in the tumor tissues of CAC mice compared with the expression in normal colon tissues. The up-regulation of H19 was also confirmed in CRC patient samples at different tumor node metastasis (TNM) stages. Moreover, H19 was associated with the stemness of colorectal cancer stem cells (CSCs) in CRC specimens. H19 promoted the stemness of CSCs and increased the frequency of tumor-initiating cells. RNA-FISH showed higher expression of H19 in tumor stroma than in cancer nests. Of note, H19 was enriched in CAF-derived conditioned medium and exosomes, which in turn promoted the stemness of CSCs and the chemoresistance of CRC cells in vitro and in vivo. Furthermore, H19 activated the β-catenin pathway via acting as a competing endogenous RNA sponge for miR-141 in CRC, while miR-141 significantly inhibited the stemness of CRC cells. Conclusion: CAFs promote the stemness and chemoresistance of CRC by transferring exosomal H19. H19 activated the β-catenin pathway via acting as a competing endogenous RNA sponge for miR-141, while miR-141 inhibited the stemness of CRC cells. Our findings indicate that H19 expressed by CAFs of the colorectal tumor stroma contributes to tumor development and chemoresistance.
ENDOSCOPIC VACUUM THERAPY FOR TREATMENT OF THE ESOPHAGOJEJUNOSTOMOSIS LEAKEGE
Authors: K Shishin, I Nedoluzhko, N Kurushkina, L Shumkina, A Pyatakova
Journal: Endoscopy (2018)

The patient of 72 y.o. suffering from stomach cancer underwent gastrectomy with the formation of an esophagojejunostomy. The diagnosis of anastomosic failure was made on the 3rd day after the operation. The endoscopic clipping of the fistula was ineffective. On the 7th day after the operation, the anastomosis diverged by 2/3 of the circumference and the leakage in the mediastinum formed.
Sitting behaviour and physical activity: two sides of the same cardiovascular health coin?
Authors: Emmanuel Stamatakis, Jason M R Gill
Journal: British Journal of Sports Medicine (2018)

Sedentary behaviour, or too much sitting, is considered an emerging risk factor for cardiovascular disease (CVD); however, little is known about its interplay with physical activity (PA). In other words, does sitting elevate CVD risk in those who are highly physically active? In this issue of BJSM, Ekelund and colleagues1 present results from a large pooled analysis on the associations between sedentary behaviour (sitting time and TV time) and cause-specific mortality across different levels of moderate to vigorous physical activity (MVPA). Here, we comment specifically on the associations of sitting time with CVD mortality in nine pooled studies including over 850 000 participants.

This very large data set1 highlights that high levels of MVPA may eliminate the associations between sitting and CVD mortality. Dose-response of CVD mortality risk with sitting was evident only in the least active quartile which corresponds to those people who undertake <5 min of MVPA per day.1 

Importantly, and good news for the many recreationally active office workers, the association of sitting with CVD death was eliminated at the top MVPA quartile (which corresponded to over approximately 65 min/day1). For the two middle quartiles (that is, those in a wide span from ≥5 through to 65 MVPA …
Disease and outcome disparities in multiple myeloma: exploring the role of race/ethnicity in the Cooperative Group clinical trials
Authors: Sikander Ailawadhi, Susanna Jacobus, Rachael Sexton, Alexander K. Stewart, Angela Dispenzieri, Mohamad A. Hussein, Jeffrey A. Zonder, John Crowley, Antje Hoering, Bart Barlogie, Robert Z. Orlowski, S. Vincent Rajkumar
Journal: Blood Cancer Journal (2018)

Abstract Multiple myeloma (MM) is an incurable hematologic malignancy with disparities in outcomes noted among racial-ethnic subgroups, likely due to disparities in access to effective treatment modalities. Clinical trials can provide access to evidence-based medicine but representation of minorities on therapeutic clinical trials has been dismal. We evaluated the impact of patient race-ethnicity in pooled data from nine large national cooperative group clinical trials in newly diagnosed MM. Among 2896 patients enrolled over more than two decades, only 18% were non-White and enrollment of minorities actually decreased in most recent years (2002–2011). African-Americans were younger and had more frequent poor-risk markers, including anemia and increased lactate dehydrogenase. Hispanics had the smallest proportion of patients on trials utilizing novel therapeutic agents. While adverse demographic (increased age) and clinical (performance status, stage, anemia, kidney dysfunction) factors were associated with inferior survival, patient race-ethnicity did not have an effect on objective response rates, progression-free, or overall survival. While there are significant disparities in MM incidence and outcomes among patients of different racial-ethnic groups, this disparity seems to be mitigated by access to appropriate therapeutic options, for example, as offered by clinical trials. Improved minority accrual in therapeutic clinical trials needs to be a priority.
Discovery of Selective Estrogen Receptor Covalent Antagonists for the Treatment of ERαWT and ERαMUT Breast Cancer
Authors: Xiaoling Puyang, Craig Furman, Guo Zhu Zheng, Zhenhua J. Wu, Deepti Banka, Kiran Aithal, Sergei Agoulnik, David M. Bolduc, Silvia Buonamici, Benjamin Caleb, Subhasree Das, Sean Eckley, Peter Fekkes, Ming-Hong Hao, Andrew Hart, René Houtman, Sean Irwin, Jaya J. Joshi, Craig Karr, Amy Kim, Namita Kumar, Pavan Kumar, Galina Kuznetsov, Weidong G. Lai, Nicholas Larsen, Crystal Mackenzie, Lesley-Ann Martin, Diana Melchers, Alyssa Moriarty, Tuong-Vi Nguyen, John Norris, Morgan O'Shea, Sunil Pancholi, Sudeep Prajapati, Sujatha Rajagopalan, Dominic J. Reynolds, Victoria Rimkunas, Nathalie Rioux, Ricardo Ribas, Amy Siu, Sasirekha Sivakumar, Vanitha Subramanian, Michael Thomas, Frédéric H. Vaillancourt, John Wang, Suzanne Wardell, Michael J. Wick, Shihua Yao, Lihua Yu, Markus Warmuth, Peter G. Smith, Ping Zhu, Manav Korpal
Journal: Cancer Discovery (2018)

Mutations in estrogen receptor alpha (ERα) that confer resistance to existing classes of endocrine therapies are detected in up to 30% of patients who have relapsed during endocrine treatments. Because a significant proportion of therapy-resistant breast cancer metastases continue to be dependent on ERα signaling, there remains a critical need to develop the next generation of ERα antagonists that can overcome aberrant ERα activity. Through our drug-discovery efforts, we identified H3B-5942, which covalently inactivates both wild-type and mutant ERα by targeting Cys530 and enforcing a unique antagonist conformation. H3B-5942 belongs to a class of ERα antagonists referred to as selective estrogen receptor covalent antagonists (SERCA). In vitro comparisons of H3B-5942 with standard-of-care (SoC) and experimental agents confirmed increased antagonist activity across a panel of ERαWT and ERαMUT cell lines. In vivo, H3B-5942 demonstrated significant single-agent antitumor activity in xenograft models representing ERαWT and ERαY537S breast cancer that was superior to fulvestrant. Lastly, H3B-5942 potency can be further improved in combination with CDK4/6 or mTOR inhibitors in both ERαWT and ERαMUT cell lines and/or tumor models. In summary, H3B-5942 belongs to a class of orally available ERα covalent antagonists with an improved profile over SoCs.Significance: Nearly 30% of endocrine therapy-resistant breast cancer metastases harbor constitutively activating mutations in ERα. SERCA H3B-5942 engages C530 of both ERαWT and ERαMUT, promotes a unique antagonist conformation, and demonstrates improved in vitro and in vivo activity over SoC agents. Importantly, single-agent efficacy can be further enhanced by combining with CDK4/6 or mTOR inhibitors. Cancer Discov; 8(9); 1176-93. ©2018 AACR.This article is highlighted in the In This Issue feature, p. 1047.
Response by Bonaca and Sabatine to Letters Regarding Article, “Low-Density Lipoprotein Cholesterol Lowering With Evolocumab and Outcomes in Patients With Peripheral Artery Disease: Insights From the FOURIER Trial (Further Cardiovascular Outcomes Research With PCSK9 Inhibition in Subjects With Elevated Risk)”
Authors: Marc P. Bonaca, Marc S. Sabatine
Journal: Circulation (2018)
Diagnosis and management of Cornelia de Lange syndrome: first international consensus statement
Authors: Antonie D. Kline, Joanna F. Moss, Angelo Selicorni, Anne-Marie Bisgaard, Matthew A. Deardorff, Peter M. Gillett, Stacey L. Ishman, Lynne M. Kerr, Alex V. Levin, Paul A. Mulder, Feliciano J. Ramos, Jolanta Wierzba, Paola Francesca Ajmone, David Axtell, Natalie Blagowidow, Anna Cereda, Antonella Costantino, Valerie Cormier-Daire, David FitzPatrick, Marco Grados, Laura Groves, Whitney Guthrie, Sylvia Huisman, Frank J. Kaiser, Gerritjan Koekkoek, Mary Levis, Milena Mariani, Joseph P. McCleery, Leonie A. Menke, Amy Metrena, Julia O’Connor, Chris Oliver, Juan Pie, Sigrid Piening, Carol J. Potter, Ana L. Quaglio, Egbert Redeker, David Richman, Claudia Rigamonti, Angell Shi, Zeynep Tümer, Ingrid D. C. Van Balkom, Raoul C. Hennekam
Journal: Nature Reviews Genetics (2018)

Cornelia de Lange syndrome (CdLS) is an archetypical genetic syndrome that is characterized by intellectual disability, well-defined facial features, upper limb anomalies and atypical growth, among numerous other signs and symptoms. It is caused by variants in any one of seven genes, all of which have a structural or regulatory function in the cohesin complex. Although recent advances in next-generation sequencing have improved molecular diagnostics, marked heterogeneity exists in clinical and molecular diagnostic approaches and care practices worldwide. Here, we outline a series of recommendations that document the consensus of a group of international experts on clinical diagnostic criteria, both for classic CdLS and non-classic CdLS phenotypes, molecular investigations, long-term management and care planning. Cornelia de Lange syndrome is a genetic disorder affecting multiple organ systems that exhibits great phenotypic heterogeneity. This Consensus Statement summarizes recommendations for the diagnosis and management of patients with Cornelia de Lange syndrome.
New Myocyte Formation in the Adult Heart
Authors: Ronald J. Vagnozzi, Jeffery D. Molkentin, Steven R. Houser
Journal: Circulation Research (2018)

Death of adult cardiac myocytes and supportive tissues resulting from cardiovascular diseases such as myocardial infarction is the proximal driver of pathological ventricular remodeling that often culminates in heart failure. Unfortunately, no currently available therapeutic barring heart transplantation can directly replenish myocytes lost from the injured heart. For decades, the field has struggled to define the intrinsic capacity and cellular sources for endogenous myocyte turnover in pursuing more innovative therapeutic strategies aimed at regenerating the injured heart. Although controversy persists to this day as to the best therapeutic regenerative strategy to use, a growing consensus has been reached that the very limited capacity for new myocyte formation in the adult mammalian heart is because of proliferation of existing cardiac myocytes but not because of the activity of an endogenous progenitor cell source of some sort. Hence, future therapeutic approaches should take into consideration the fundamental biology of myocyte renewal in designing strategies to potentially replenish these cells in the injured heart.
Regional Adipose Distribution and its Relationship to Exercise Intolerance in Older Obese Patients Who Have Heart Failure With Preserved Ejection Fraction
Authors: Mark J Haykowsky, Barbara J Nicklas, Peter H Brubaker, W Gregory Hundley, Tina E Brinkley, Bharathi Upadhya, J Thomas Becton, Michael D Nelson, Haiying Chen, Dalane W Kitzman
Journal: JACC Heart Failure (2018)
TUBERCULOSIS LYMPH NODE PRESENTING AS A CYSTIC MASS OF THE PANCREATIC HEAD
Authors: A Taiymi, W Khannoussi, S Naji, A El Mekkaoui, G Kharrasse, Z Ismaili
Journal: Endoscopy (2018)

A 31-years-old man, active smoker with no history of tuberculosis, presented an atypical epigastralgia during one month, associated with asthenia and apyrexia. Abdominal examination found epigastric sensitivity. There was no peripheral adenomegalies found. The results of hematological tests were WBC 11900/mm3 and lymphocytes at 3660/mm3, CRP was at 93 mg/l. Liver enzymes were normal except from GGT (2.2N). Abdominal ultrasound found many peripancreatic and hepatic adenopathies and a cystic lesion of the pancreatic head. CT scan found the same and a thickening of the ileum. We suspected a digestive and lymphatic tuberculosis. Tuberculin intradermoreaction test was positive (20 mm) and chest X-ray was negative. Ileocolonoscopy showed superficial small ulcerations of the ileum, pathology examination couldn't confirm tuberculosis origin. CP MRI confirmed the presence of peripancreatic adenopathies and a 5 cm cystic mass adjacent to the pancreatic head with no communication with the main pancreatic duct and homogenous content. Endoscopic ultrasound showed the presence of a polycyclic lesion with heterogeneous liquid content measuring 3 × 5 cm along the hepatic pedicle and coming into contact with the pancreatic isthmus; this lesion was surrounded by multiple adenopathies. The results of fine needle aspiration (FNA) with 22 G needle were the presence of inflammatory material with suppurative necrosis. There were no epitheliod cell granulomas. The detection of Mycobacterium tuberculosis DNA by PCR in the materiel of FNA was positive. The diagnosis of abdominal lymph nodes tuberculosis was established and anti bacillary treatment was started.
Reducing protein oxidation reverses lung fibrosis
Authors: Vikas Anathy, Karolyn G. Lahue, David G. Chapman, Shi B. Chia, Dylan T. Casey, Reem Aboushousha, Jos L. J. van der Velden, Evan Elko, Sidra M. Hoffman, David H. McMillan, Jane T. Jones, James D. Nolin, Sarah Abdalla, Robert Schneider, David J. Seward, Elle C. Roberson, Matthew D. Liptak, Morgan E. Cousins, Kelly J. Butnor, Douglas. J. Taatjes, Ralph C. Budd, Charles G. Irvin, Ye-Shih Ho, Razq Hakem, Kevin K. Brown, Reiko Matsui, Markus M. Bachschmid, Jose L. Gomez, Naftali Kaminski, Albert van der Vliet, Yvonne M. W. Janssen-Heininger
Journal: Nature Medicine (2018)
Low-Fat vs Low-Carbohydrate Diets and Weight Loss—Reply
Authors: Christopher Gardner
Journal: JAMA (2018)

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Binding of Dickkopf-3 to CXCR7 Enhances Vascular Progenitor Cell Migration and Degradable Graft Regeneration
Authors: Shirin Issa Bhaloo, Yifan Wu, Alexandra Le Bras, Baoqi Yu, Wenduo Gu, Yao Xie, Jiacheng Deng, Zhihong Wang, Zhongyi Zhang, Deling Kong, Yanhua Hu, Aijuan Qu, Qiang Zhao, Qingbo Xu
Journal: Circulation Research (2018)

Vascular progenitor cells play key roles in physiological and pathological vascular remodeling-a process that is crucial for the regeneration of acellular biodegradable scaffolds engineered as vital strategies against the limited availability of healthy autologous vessels for bypass grafting. Therefore, understanding the mechanisms driving vascular progenitor cells recruitment and differentiation could help the development of new strategies to improve tissue-engineered vessel grafts and design drug-targeted therapy for vessel regeneration.In this study, we sought to investigate the role of Dkk3 (dickkopf-3), recently identified as a cytokine promotor of endothelial repair and smooth muscle cell differentiation, on vascular progenitor cells cell migration and vascular regeneration and to identify its functional receptor that remains unknown.Vascular stem/progenitor cells were isolated from murine aortic adventitia and selected for the Sca-1 (stem cell antigen-1) marker. Dkk3 induced the chemotaxis of Sca-1+ cells in vitro in transwell and wound healing assays and ex vivo in the aortic ring assay. Functional studies to identify Dkk3 receptor revealed that overexpression or knockdown of chemokine receptor CXCR7 (C-X-C chemokine receptor type 7) in Sca-1+ cells resulted in alterations in cell migration. Coimmunoprecipitation experiments using Sca-1+ cell extracts treated with Dkk3 showed the physical interaction between DKK3 and CXCR7, and specific saturation binding assays identified a high-affinity Dkk3-CXCR7 binding with a dissociation constant of 14.14 nmol/L. Binding of CXCR7 by Dkk3 triggered the subsequent activation of ERK1/2 (extracellular signal-regulated kinases 1/2)-, PI3K (phosphatidylinositol 3-kinase)/AKT (protein kinase B)-, Rac1 (Ras-related C3 botulinum toxin substrate 1)-, and RhoA (Ras homolog gene family, member A)-signaling pathways involved in Sca-1+ cell migration. Tissue-engineered vessel grafts were fabricated with or without Dkk3 and implanted to replace the rat abdominal aorta. Dkk3-loaded tissue-engineered vessel grafts showed efficient endothelization and recruitment of vascular progenitor cells, which had acquired characteristics of mature smooth muscle cells. CXCR7 blocking using specific antibodies in this vessel graft model hampered stem/progenitor cell recruitment into the vessel wall, thus compromising vascular remodeling.We provide a novel and solid evidence that CXCR7 serves as Dkk3 receptor, which mediates Dkk3-induced vascular progenitor migration in vitro and in tissue-engineered vessels, hence harnessing patent grafts resembling native blood vessels.