tbuckley/cabot-search huggingface dataset:
O026 Which place for the NLRP3 inflammasome in the MSU crystal-induced inflammatory response in vivo?
Authors: A Mariotte, Z Zhang, A de Cauwer, B Frisch, S Bahram, R Ricci, P Georgel
Journal: Annals of the Rheumatic Diseases (2018)

<h3>Introduction</h3> The NLRP3 (<b><i>N</i></b><i>ucleotide-binding and oligomerisation domain, <b>L</b>eucine-<b>R</b>ich repeat and <b>P</b>yrin containing <b>3</b></i>) inflammasome is a multiprotein complex made of the NLRP3 sensor, the caspase 1 enzyme and an adaptor, ASC. Upon exposure to sterile or infectious stimuli, the NLRP3 inflammasome assembles and cleaves pro-IL-1β and pro-IL-18 into their bioactive forms. Gout is a common microcrystalline arthritis induced by MSU (<b>M</b>ono-<b>S</b>odium <b>U</b>rate) crystals accumulation which triggers an inflammatory response depending on the NLRP3-IL-1-IL-1R axis <i>in vitro</i><sup>1</sup>; however, this relationship is far less understood <i>in vivo</i>. PKD (<b><i>P</i></b><i>rotein <b>K</b>inase <b>D</b></i>) were recently shown as important regulators of the NLRP3 inflammasome.<sup>2</sup> <h3>Objectives</h3> To study the <i>in vivo</i> relevance of the PKDs-NLRP3 axis in two mouse models of gout. <h3>Methods</h3> Experiments were conducted in mice deficient for NLRP3, for PKD1 and 3 or mice in which PKD1, 2 and 3 were blocked by a pan-PKD inhibitor. Peritoneal macrophages were stimulated by MSU crystals to assess IL-1β production. Gouty arthritis was triggered by subcutaneous injections of MSU crystals in the hind-paws and MSU-induced peritonitis by crystals injection in the peritoneal cavity. <h3>Results</h3> We confirmed the absence of IL1β release by MSU-challenged peritoneal macrophages isolated from NLRP3KO animals. Pharmacological pan-PKD inhibition gave similar results, whereas genetic loss of PKD1 and 3 did not. The peritoneal gout model showed a reduction in neutrophils recruitment in NLRP3KO animals, and an increased neutrophils influx in PKD1-3dKO mice. Finally, we did not observe any alteration in gout severity in NLRP3-deficient and pan-PKD inhibitor-treated mice following MSU crystal subcutaneous injections; PKD1-3dKO animals even displayed more severe symptoms in this assay. <h3>Conclusions</h3> Our data seem to confirm that the PKD-NLRP3 axis exerts a major role in sensing MSU crystals <i>in vitro</i> but the relevance of this pathway in our <i>in vivo</i> gouty arthritis models is not so clear. We speculate that an alternative pathway could compensate for the loss of IL-1β in NLRP3 inflammasome-deficient mice. Unravelling this possibility might be of major fundamental interest and could even lead to new therapeutics in the field of inflammation. <h3>References</h3> . Martinon F, et al. Nature2006. . Zhang Z, et al<i>. J. Exp. Med</i>2017. <h3>Disclosure of interest</h3> None declared
MicroRNA 15a/16‐1 suppresses aryl hydrocarbon receptor–dependent interleukin‐22 secretion in CD4+ T cells and contributes to immune‐mediated organ injury
Authors: Zhou Lu, Jiajing Liu, Xiaoming Liu, Enyu Huang, Jiao Yang, Jiawen Qian, Dan Zhang, Ronghua Liu, Yiwei Chu
Journal: Hepatology (2017)

Interleukin‐22 (IL‐22), as a link between leukocytic and nonleukocytic cells, has gained increasing attention for its pronounced tissue‐protective properties. MicroRNAs, emerging as crucial immune modulators, have been reported to be involved in the production and action of various cytokines. However, the precise control of IL‐22 by microRNAs and its subsequent actions remained to be elucidated. In this study, we found a negative correlation between the expression of microRNA 15a/16‐1 (miR‐15a/16‐1) and IL‐22 in the model of concanavalin A–induced, immune‐mediated liver injury. Knockout of miR‐15a/16‐1 ameliorated liver injury in an IL‐22‐dependent manner. Further results revealed that cluster of differentiation 4–positive (CD4 + ) T cells were the major source of IL‐22 during liver injury and that the aryl hydrocarbon receptor was the direct target of miR‐15a/16‐1 in CD4 + T cells. In vivo and in vitro data showed that miR‐15a/16‐1 knockout CD4 + T cells produced more IL‐22, while overexpression of miR‐15a/16‐1 down‐regulated the IL‐22 production by inhibiting the aryl hydrocarbon receptor. Moreover, transfer of miR‐15a/16‐1 knockout CD4 + T cells promoted tissue repair compared to wild‐type CD4 + T cells by up‐regulating IL‐22. In addition, as a synergistic effect, IL‐22 could down‐regulate miR‐15a/16‐1 expression by activating phosphorylated signal transducer and activator of transcription 3‐c‐myc signaling, and the decrease of miR‐15a/16‐1 in damaged hepatocytes contributed to IL‐22‐mediated tissue repair by reducing cell apoptosis and promoting cell proliferation. As further proof, we demonstrated the role of miR‐15a/16‐1 in controlling IL‐22 production and IL‐22‐mediated reconstruction of the intestinal epithelial barrier in a dextran sodium sulfate–induced colitis model. Conclusion : Our results suggest that miR‐15a/16‐1 acts as a essential regulator of IL‐22 and that the miR‐15a/16‐1–aryl hydrocarbon receptor–IL‐22 regulatory axis plays a central role in tissue repair; modulation of miR‐15a/16‐1 might hold promise in developing new strategies to enhance IL‐22‐mediated tissue repair. (H epatology 2018;67:1027–1040)
Treatment patterns for metastatic hormone-sensitive prostate cancer (mHSPC) progressing after up-front docetaxel in combination with androgen deprivation therapy (D-ADT).
Authors: Pedro C. Barata, Hamid Emamekhoo, Prateek Mendiratta, Dharmesh Gopalakrishnan, Vadim S. Koshkin, Allison Janine Tyler, Moshe Chaim Ornstein, Petros Grivas, Timothy D. Gilligan, Brian I. Rini, Christos Kyriakopoulos, Jorge A. Garcia
Journal: Journal of Clinical Oncology (2018)

305 Background: D-ADT increases overall survival (OS) in men with mHSPC. All patients (pts) however progress and develop castration-resistant prostate cancer (CRPC). Little is known about response to subsequent therapy and outcomes in this setting. Methods: Retrospective analysis of consecutive mHSPC pts treated with ≥3 cycles of D-ADT at Cleveland Clinic and University of Wisconsin-Madison. We aimed to describe baseline, progression characteristics, treatment choices, sequence and outcome of subsequent therapy. Results: A total of 146 mHSPC pts were treated with D-ADT (6% 1-2 cycles; 94% ≥3 cycles). Final analysis included 136 pts, median age 65 (range 35-86), 65% GS≥8, 79% high-volume disease. Median number of D cycles was 6 (1-6). PSA declined to “0” at 12 and 24 months in 32% and 25% of pts, respectively. Median time to CRPC (biochemical, clinical or radiographic) was 19.6 months (95% CI, 16.6-22.6). 57 pts (42%) received ≥1 subsequent treatment after CRPC [46 hormonal therapy (HT) (21 abiraterone acetate, 19 enzalutamide, 6 ASN-001); 4 Sipuleucel-T; 4 radium-223, 5 chemotherapy (2 carboplatin-based, 2 cabazitaxel, 1 D); 3 temsirolimus/bevacizumab]. Treatment response was independent from time to CRPC (≥12 months, p = 0.264). Pts receiving HT as the first subsequent treatment had a median rPFS of 13.3 months (95% CI, 10.1-16.5) compared with 3.1 months (95% CI, 0-15.8) for non-HT (p = 0.332). Treatment choice was independent of GS (p = 0.513), visceral disease (p = 0.374) and time to CRPC (p = 0.500). Most CRPC pts treated with ≥2 lines of therapy received one HT (n = 21) followed by a different HT (43%), chemo (38%), radium-223 (14%) or olaparib (10%). 57% of pts were alive at 2 years. Longer OS correlated with time to CRPC (p = 0.010) and first subsequent treatment with HT (p = 0.009) but not with visceral disease (p = 0.258), GS (p = 0.599) or sequence of therapies received (HT/HT vs HT/non-HT, p = 0.836). Conclusions: Prior D-ADT did not preclude subsequent treatment response in CRPC pts, independent of time to CRPC. The choice of first-line treatment for CRPC may impact survival in favor of those who start HT.
Abstract P4-02-12: Predicting surgical upgrade of breast lesions detected by MRI-guided biopsy
Authors: A Chen, R Brem
Journal: Cancer Research (2018)

Abstract Background: Patients who have suspicious breast lesions identified with MRI without mammographic- or ultrasound-correlated biopsy require MRI-guided biopsy. However, MRI-guided biopsy may underestimate the pathology due to intrinsic heterogeneity, in which subsequent surgical excision may reveal an upgrade. The reported upgrade rate is variable across studies, subclasses of lesion, and needle gauge, and no associative factors have been identified. This study investigated demographic and histologic characteristics of lesions that underwent MRI-guided biopsy to determine possible factors for predicting later upgrade at surgery. Methods: All MRI-guided vacuum biopsies performed between 2012 and 2017 at GWU Breast Imaging Center were reviewed. Surgical excision was performed for high risk lesions and imaging discordance in benign lesions. Variables investigated include patient age, menopausal status, personal/family history of breast cancer and breast pathology. T-test and Pearson's chi-squared test were used to determine statistical significance (alpha=0.05). Results: Of 379 lesions from 295 patients that underwent MRI-guided biopsy, 117 lesions from 96 patients underwent subsequent surgical excision. Pathology of the 117 lesions included benign (14/117; 12%), ALH (17/117; 15%), LCIS (10/117; 9%), ADH (10/117; 9%), papilloma (25/117; 21%), radial scar (12/117; 10%), DCIS (13/117; 11%), invasive cancer (10/117; 9%), and others (6/117; 5%). 14 of 117 lesions (12%) were upgraded at surgery: 5 upgraded from benign to high-risk, 1 upgraded from benign to DCIS, 4 upgraded from high risk to DCIS, 1 upgraded from high risk to invasive cancer and 3 upgraded from DCIS to invasive cancer. All 14 patient with upgrades (100%) had a personal history of breast cancer. No association was found with age, menopausal status, breast pathology, or family history. Conclusions: Our study demonstrated a surgical upgrade rate of 12%. All upgrades occurred in women with a personal history. We suggest that patients with a personal history of breast cancer pose a higher risk of surgical upgrade at excision. Citation Format: Chen A, Brem R. Predicting surgical upgrade of breast lesions detected by MRI-guided biopsy [abstract]. In: Proceedings of the 2017 San Antonio Breast Cancer Symposium; 2017 Dec 5-9; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2018;78(4 Suppl):Abstract nr P4-02-12.
Abstract P1-01-17: Characterization of novel ESR1 (c.749T&amp;gt;C; p.Met250Thr) mutation in enhancing cellular invasiveness of breast cancer
Authors: N Liao, G-C Zhang, Y Wang, L Cao, K Li, C-Y Ren, L-Z Wen, Y Shi, W Zhu, X Chen
Journal: Cancer Research (2018)

Abstract Emerging evidence has revealed that the mutations in estrogen receptor alpha (ERα) gene (ESR1) is frequently observed in ER+ metastatic breast cancer, and is associated with the aggressively invasive and metastatic phenotype in advanced breast cancer due to the resistance of endocrine therapy. In our previous study, we have identified three novel mutations of ESR1, including ESR1 G74R, D230H and M250T, in the untreated patients with early breast cancer. However, the functional roles for these novel mutations in the cellular biology of breast cancer remain to be elucidated. In this study, we described the molecular mechanism underlying potential roles for the novel mutation ESR1 p.Met250Thr (c.749T&amp;gt;C) in regulating the cellular invasiveness of breast cancer. Firstly, we found, as compared with wild-type (WT) HA-ESR1, forced expression of HA-ESR1 M250T enhanced the invasive capacity of breast cancer MCF-7 cells by using Transwell assay. Moreover, we found that the levels of miR-190 were significantly up-regulated in the MCF-7 (HA-ESR1 M250T) cells, and further verified that miR-190 played an important role in ESR1 M250T-mediated induction of cellular invasiveness by using specific shRNA to knock down miR-190 levels in MCF-7 (HA-ESR1 M250T) cells. Further bioinformatics analysis showed that there were several half Estrogen Response Elements (EREs) in the promoter region of Talin-2, as the host gene of miR-190. Talin-2-driven luciferase reporter assay indicated ESR1 M250T resulted in a higher increase in the luciferase activity than ESR1 WT. Chromatin-immunoprecipitation (ChIP) assay identified a higher binding ability with Talin-2 promoter for ESR1 M250T than ESR1 WT. Collectively, our mechanistic study revealed that the ESR1 M250T mutation, located in the DNA-binding domain, increased the invasive capacity of breast cancer cells via the transcriptional induction of Talin-2 and miR-190. The potential role for ESR1 M250T in affecting the efficacy of endocrine therapy has been under the investigation in our laboratory, and the result from which will help us better elucidate the clinical relevance for novel ESR1 mutations in affecting the sensitivity of endocrine therapy. This study was supported in part by National Natural Science Foundation of China (8160111571) and Guangdong Natural Science Foundation (2016A030313768). Citation Format: Liao N, Zhang G-C, Wang Y, Cao L, Li K, Ren C-Y, Wen L-Z, Shi Y, Zhu W, Chen X. Characterization of novel ESR1 (c.749T&amp;gt;C; p.Met250Thr) mutation in enhancing cellular invasiveness of breast cancer [abstract]. In: Proceedings of the 2017 San Antonio Breast Cancer Symposium; 2017 Dec 5-9; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2018;78(4 Suppl):Abstract nr P1-01-17.
USEFULNESS OF POSITIONAL ANGIOGRAPHY AND CATHETERIZATION STUDY: A CASE OF PLATYPNEA-ORTHODEOXIA SYNDROME SUCCESSFULLY TREATED WITH TRANSCUTANEOUS FORAMEN OVALE CLOSURE
Authors: Kazuhiro Kuroda, Gentaro Shokoku, Keisuke Yamamoto, Tamaki Ono, Koji Tokioka, Yusuke Kawai, Teiji Akagi, Hiroshi Ito, Tohru Ohe
Journal: Journal of the American College of Cardiology (2018)
METABOLICALLY HEALTHY AND UNHEALTHY OBESITY AND CHANGES IN LEFT VENTRICULAR MASS, VOLUME AND FUNCTION BY CARDIAC MAGNETIC RESONANCE IMAGING: RESULTS FROM THE MULTI-ETHNIC STUDY OF ATHEROSCLEROSIS
Authors: Diana Glovaci, David A. Bluemke, Matthew Budoff, Laurence Sperling, Dan Gaita, Morgana Mongraw-Chaffin, Maria E.P. Trejo, Matthew Allison, Nathan Wong
Journal: Journal of the American College of Cardiology (2018)
HISTOLOGICAL QUANTIFICATION OF RIGHT VENTRICULAR MYOCARDIAL FIBROSIS AND ITS IMPACT ON RIGHT VENTRICULAR REVERSE REMODELING IN ADULT PATIENTS WITH REPAIRED TETRALOGY OF FALLOT
Authors: Kenichiro Yamamura, Darren Yuen, Edward Hickey, Rajiv Chaturvedi, Mark Friedberg, Rachel Wald
Journal: Journal of the American College of Cardiology (2018)
Association of Prenatal Ultrasonography and Autism Spectrum Disorder
Authors: N. Paul Rosman, Rachel Vassar, Gheorghe Doros, James DeRosa, Allison Froman, Audrey DiMauro, Sherry Santiago, Jodi Abbott
Journal: JAMA Pediatrics (2018)

The prevalence of autism spectrum disorder (ASD) has been increasing rapidly, with current estimates of 1 in 68 children affected. Simultaneously, use of prenatal ultrasonography has increased substantially, with limited investigation into its safety and effects on brain development. Animal studies have demonstrated that prenatal ultrasonography can adversely affect neuronal migration.
UPDATE OF A COMPARISON OF RADIATION DOSE BETWEEN CONTEMPORARY FLUOROSCOPY SYSTEMS USING AN ANTHROPOMORPHIC PHANTOM IN THE CARDIAC CATHETERIZATION LABORATORY
Authors: Jose Martinez Parachini, Judit Karacsonyi, Tayo Addo, Vasiliki Dimas, Michael Luna, Bavana Rangan, Peter Tajti, Ronald Layne, Donald Haagen, Houman Khalili, Subhash Banerjee, Emmanouil Brilakis
Journal: Journal of the American College of Cardiology (2018)
Forkhead Box F2 Suppresses Gastric Cancer through a Novel FOXF2–IRF2BPL–β-Catenin Signaling Axis
Authors: Akira Higashimori, Yujuan Dong, Yanquan Zhang, Wei Kang, Geicho Nakatsu, Simon S.M. Ng, Tetsuo Arakawa, Joseph J.Y. Sung, Francis K.L. Chan, Jun Yu
Journal: Cancer Research (2018)

DNA methylation has been identified as a hallmark of gastric cancer (GC). Identifying genes that are repressed by DNA promoter methylation is essential in providing insights into the molecular pathogenesis of gastric cancer. Using genome-wide methylation studies, we identified that transcription factor forkhead box F2 (FOXF2) was preferentially methylated in gastric cancer. We then investigated the functional significance and clinical implication of FOXF2 in gastric cancer. FOXF2 was silenced in gastric cancer cell lines and cancer tissues by promoter methylation, which was negatively associated with mRNA expression. Ectopic expression of FOXF2 inhibited proliferation, colony formation, G1-S cell-cycle transition, induced apoptosis of gastric cancer cell lines, and suppressed growth of xenograft tumors in nude mice; knockdown of FOXF2 elicited opposing effects. FOXF2 inhibited Wnt signaling by inducing β-catenin protein ubiquitination and degradation independently of GSK-3β. FOXF2 directly bound the promoter of E3 ligase interferon regulatory factor 2-binding protein-like (IRF2BPL) and induced its transcriptional expression. IRF2BPL in turn interacted with β-catenin, increasing its ubiquitination and degradation. Multivariate Cox regression analysis identified FOXF2 hypermethylation as an independent prognostic factor of poor survival in early-stage gastric cancer patients. In conclusion, FOXF2 is a critical tumor suppressor in gastric carcinogenesis whose methylation status serves as an independent prognostic factor for gastric cancer patients.Significance: FOXF2-mediated upregulation of the E3 ligase IRF2BPL drives ubiquitylation and degradation of β-catenin in gastric cancer, blunting Wnt signaling and suppressing carcinogenesis. Cancer Res; 78(7); 1643-56. ©2018 AACR.
Working in New Zealand—a positive experience
Authors: Paul Grant
Journal: BMJ (2004)

After our house jobs and before the joys of membership and mortgages, my partner and I decided to leave the United Kingdom and take the mighty leap down under. It had always been our ambition to live and work in New Zealand. We had no trouble securing jobs in the South Canterbury region of South Island. Our New Zealand doctor friends told us that the hospital had a good reputation, and the hospital trust even sent us a promotional video.

When we started our jobs as second year house surgeons we were instantly impressed with the hospital set up. New Zealand is a naturally friendly place and its health service—for patients and doctors—seems light years ahead of the NHS. We were acutely aware of this, having just been through the stresses and strains of the pre-registration house officer year in the NHS.

New Zealand is a naturally friendly place

Our induction week, for example, was outstanding. The chief …
Allele-Specific Mechanisms of Activation of MEK1 Mutants Determine Their Properties
Authors: Yijun Gao, Matthew T. Chang, Daniel McKay, Na Na, Bing Zhou, Rona Yaeger, Neilawattie M. Torres, Keven Muniz, Matthias Drosten, Mariano Barbacid, Giordano Caponigro, Darrin Stuart, Henrik Moebitz, David B. Solit, Omar Abdel-Wahab, Barry S. Taylor, Zhan Yao, Neal Rosen
Journal: Cancer Discovery (2018)

Mutations at multiple sites in MEK1 occur in cancer, suggesting that their mechanisms of activation might be different. We analyzed 17 tumor-associated MEK1 mutants and found that they drove ERK signaling autonomously or in a RAS/RAF-dependent manner. The latter are sensitive to feedback inhibition of RAF, which limits their functional output, and often cooccur with RAS or RAF mutations. They act as amplifiers of RAF signaling. In contrast, another class of mutants deletes a hitherto unrecognized negative regulatory segment of MEK1, is RAF- and phosphorylation-independent, is unaffected by feedback inhibition of upstream signaling, and drives high ERK output and transformation in the absence of RAF activity. Moreover, these RAF-independent mutants are insensitive to allosteric MEK inhibitors, which preferentially bind to the inactivated form of MEK1. All the mutants are sensitive to an ATP-competitive MEK inhibitor. Thus, our study comprises a novel therapeutic strategy for tumors driven by RAF-independent MEK1 mutants.Significance: Mutants with which MEK1 mutants coexist and their sensitivity to inhibitors are determined by allele-specific properties. This study shows the importance of functional characterization of mutant alleles in single oncogenes and identifies a new class of MEK1 mutants, insensitive to current MEK1 inhibitors but treatable with a new ATP-competitive inhibitor. Cancer Discov; 8(5); 648-61. ©2018 AACR.See related commentary by Maust et al., p. 534This article is highlighted in the In This Issue feature, p. 517.
Abstract 13860: Patient and Partner (P+P) Intervention to Improve Outcomes After and Implantable Cardioverter Defibrillator (ICD): Three Month Physical Health Outcomes
Authors: Cynthia M Dougherty, Elaine A Thompson, Adrian Dobra, Peter J Kudenchuk
Journal: Circulation (2016)

Introduction: Partners of patients who get an ICD play a pivotal role in the patient’s adjustment over the initial 3 months. The purpose of this study was to compare 2 intervention programs after an initial ICD: an intervention for the patient-only (P) was compared to an intervention involving both the patient and their intimate partner (P+P). Hypothesis: The P+P intervention will demonstrate better patient reported outcomes than the (P)-only intervention. Methods: A prospective randomized control trial (RCT) comparing 2 interventions after an initial ICD on patient and partner outcomes, was conducted with 301 intimate couples in the Pacific NW. The self-efficacy based nurse telephone intervention was delivered over the 1 st 12 weeks following ICD implant for primary (60%) or secondary (40%) prevention. Patient physical health outcomes were measured at baseline hospital discharge and 3 months later using the Patient Concerns Assessment (PCA), SF-36 PCS, total steps taken on a Step Watch physical activity monitor, and the Sudden Cardiac Arrest Self-Efficacy (SCA-SE) scale. Structural equation modeling was used to test the hypothesized effects of the intervention and the mediating effects of self-efficacy on patient physical health. Results: ICD patients (N=150) in P-only were (mean±SD) 65.0±12.3 years old, 90.1% Caucasian, 70.2% were male, with Charlson scores of 2.26±1.4, EF% 33.8±13.5, &amp; household income $30-49,000 (23%). ICD patients (N=151) in P+P were 63.3±12.5 years old, 92% Caucasian, 77.3% were male, with Charlson scores of 2.2±1.5, EF% 34.4±15.2. From baseline to 3 months, PCA symptoms were reduced in both groups p=0.84, and SF-36 physical health (p=0.62) and total steps/day (p=0.26) improved in both groups. The direct effect of the intervention on patient self-efficacy at 3 months was significant ( B =0.11, p=0.03). Improvements in patient self-efficacy were associated with a reduction in 3 month physical symptoms ( B =-0.19, p&lt;0.001), and improved physical health ( B =0.16, p&lt;0.001), but not total steps/day ( B =0.07, p=0.07). Fit indicies met standards for model fit: CFI=0.90, RMSEA=0.08. Conclusions: The intervention arm involving the partner (P+P) resulted in higher levels of patient physical health after an initial ICD.
LONG-TERM SURVIVAL AFTER MYOCARDIAL INFARCTION IN A SIX-YEAR FOLLOW-UP COHORT, EOLE
Authors: Nicholas Moore, Cecile Droz-Perroteau, Patrick Blin, Caroline Dureau-Pournin, Daniel Thomas, Nicolas Danchin, Jacques Tricoire, Francois Paillard, Serge Hercberg, Marie-Agnes Bernard, Jacques Benichou
Journal: Journal of the American College of Cardiology (2018)
Rise in Scotland’s consultant vacancies is “extremely worrying,” says BMA
Authors: Abi Rimmer
Journal: BMJ (2014)

The BMA has called on the Scottish government to urgently tackle the rising number of vacant consultancy posts in Scotland.

The call came after a report by Information Services Division (ISD) Scotland showed that, at the end of June 2014, 6.9% of consultant posts were vacant—up from 6.5% in March 2014 and 4.7% in June 2013.1 The …
FEATURES OF NEOINTIMAL MORPHOLOGY OBSERVED BY OPTICAL COHERENCE TOMOGRAPHY BEYOND 3 YEARS AFTER EVEROLIMUS ELUTING STENT IMPLANTATION
Authors: Taishi Yonetsu, Rikuta Hamaya, Hiroaki Ohya, Yohei Sumino, Tadashi Fukuda, Masahiro Hada, Eisuke Usui, Masahiro Hoshino, Yoshihisa Kanaji, Tsunekazu Kakuta
Journal: Journal of the American College of Cardiology (2018)