tbuckley/cabot-search huggingface dataset:
TCT-610 Long-Term Outcomes of Complete Versus Incomplete Revascularization After Drug-Eluting Stent Implantation in Patients with Multivessel Coronary Disease
Authors: Zhan Gao, Bo Xu, Yuejin Yang, Shubin Qiao, Hongbing Yan, Yongjian Wu, Xuewen Qin, Min Yao, Haibo Liu, Jinqing Yuan, Jue Chen, Jun Dai, Tao Chen, Siyong Teng, JiLin Chen, Run-Lin Gao
Journal: Journal of the American College of Cardiology (2012)
TCTAP C-129 Percutaneous Coronary Intervention in Patient with Unstable Angina and Abdominal Aortic Aneurysm Supported by 6-French Intra-Aortic Balloon Pumping via Brachial Artery Using 6-French Slender Sheath
Authors: Takeshi Yamada, Akihiko Takahashi, Yukio Mizuguchi, Norimasa Taniguchi
Journal: Journal of the American College of Cardiology (2015)
The Clinical Use of Nor-Epinephrine in the Treatment of Shock Accompanying Myocardial Infarction and Other Conditions
Authors: George S. Kurland, Monte Malach
Journal: New England Journal of Medicine (1952)

THE recent availability of pure L-nor-epinephrine (arterenol, nor-adrenaline) has permitted evaluation of its clinical usefulness as a pressor agent. Preliminary reports1 2 3 4 5 6 7 have suggested beneficial results after its use in the treatment of peripheral vascular collapse. The purpose of this paper is to describe our experience with the drug, particularly in the successful treatment of shock accompanying acute myocardial infarction.Pharmacologic PropertiesNor-epinephrine (aminoethanol catechol) is a sympathomimetic primary amine, first synthesized by Stoltz8 in 1904. It can be distinguished from epinephrine by chemical, chromatographic and physiologic methods.9 The formulas are shown in Figure 1. Naturally occurring nor-epinephrine has been identified as . . .
Abstract B3: Potential new mechanism whereby IGFBP-5 contributes to cancer progression: Binding of GADD34 and enhancement of eIF2α dephosphorylation
Authors: Penny PY Ho, Steve Grkovic, Sue M. Firth
Journal: Cancer Research (2009)

Abstract Insulin-like Growth Factor Binding Protein (IGFBP-5) has a well-defined role in normal mammary gland physiology and has recently been shown to play an important role in the biology of breast cancer; however the IGF-independent mechanisms of action remain obscure. Over-expression of IGFBP-5, but not the addition of the exogenous protein, has been shown to inhibit the growth of breast cancer cells in vitro. This suggests novel intracellular mechanisms where IGFBP-5 interacts with unidentified binding partners and thereby modulates the proliferation and survival of breast cancer cells. To address this issue, we performed a yeast two-hybrid screen utilizing a normal human mammary gland cDNA library and full-length IGFBP-5 as the bait. The pre-eminent binding partner identified was Growth Arrest and DNA Damage-inducible protein 34 (GADD34), which assembles an eukaryotic initiation factor 2 alpha subunit (eIF2α) dephosphorylation complex at the endoplasmic reticulum (ER). We have confirmed that IGFBP-5 and GADD34 interact through coimmunoprecipitation experiments using ectopically expressed IGFBP-5 and GADD34 in mammalian cells. We have also shown that IGFBP-3, which belongs to the same protein family as IGFBP-5, interacts with GADD34 through coimmunoprecipitation studies. Furthermore, IGFBP-5 or IGFBP-3 expression was found to dramatically increase GADD34 protein levels as demonstrated through immunoblot analysis. However, IGFBP-2, another protein related to IGFBP-5, did not interact with GADD34 or increase its protein expression. Because GADD34-mediated eIF2α dephosphorylation is required to promote resumption of protein translation after periods of ER stress, we next examined eIF2α phosphorylation levels in the presence and absence of IGFBPs. Expression of IGFBP-5 or IGFBP-3 decreased the levels of phosphorylated eIF2α, suggesting that the interactions diminish the magnitude and/or duration of ER stress-induced inhibition of translation. Our results demonstrate not only a physical interaction between IGFBP-5 or IGFBP-3 and GADD34, but also show that these IGFBPs appear to increase the stability and activity of GADD34. This discovery suggests a novel role for IGFBP-5 and IGFBP-3 in the regulation of a protective mechanism induced by ER stress. Since ER stress is one of the hallmarks of solid tumor progression, by modifying the tumor response to hostile microenvironments, it is likely that these IGFBPs can have significant impact on cancer growth, survival, and apoptosis. Citation Information: Cancer Res 2009;69(23 Suppl):B3.
Abstract 1855: Jab1/CSN5 a negative regulator of p27 plays a role in the pathogenesis and cisplatin sensitivity of nasopharyngeal carcinoma
Authors: Yunbao Pan, Qingxiu Zhang, Ling Tian, Xin Wang, Xiaohang Fan, Huizhong Zhang, Huiling Yang, Francois X. Claret
Journal: Cancer Research (2012)

Abstract Nasopharyngeal carcinoma (NPC) is an Epstein-Barr virus-associated malignancy most common in East Asia and Africa. Previous studies have reported that genetic susceptibility is associated with NPC. Jab1/CSN5 promotes cell growth and proliferation. Recent studies have shown that Jab1/CSN5 is aberrantly expressed, is correlated with low expression of p27, and is associated with advanced tumor stage and poor prognosis in several human cancers. In this study, we examined the functional role and correlation between Jab1/CSN5 and p27 protein expression in NPC tissue samples and cell lines, the association of their expression with clinical outcome and the antitumor effects of cisplatin in NPC cells. Immunohistochemical analysis showed that Jab1/CSN5 aberrant expression was inversely associated with p27 expression in NPC tissue samples, and Jab1/CSN5 overexpression was correlated with poor survival (p&amp;lt;0.01). Further analysis showed that Jab1/CSN5 mediated p27 degradation in a proteasome-dependent manner, and Jab1/CSN5 directly interacted with p27 in NPC cells. In addition, inactivation of Jab1/CSN5 by small interfering RNAs resulted in a remarkable increase in p27 levels and in the inhibition of cell proliferation, thereby indicating that Jab1/CSN5 controls the stability of p27 by targeting it for degradation in NPC. Moreover, suppression of Jab1/CSN5 enhanced the antitumor effects of cisplatin in NPC cells. To our knowledge, these findings are the first to suggest that Jab1/CSN5 overexpression is involved in NPC pathogenesis via Jab1-mediated p27 degradation, thus explaining the low p27 levels seen in NPC. Therefore, Jab1/CSN5 could be a diagnostic marker and a novel therapeutic target in patients with NPC. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 1855. doi:1538-7445.AM2012-1855
FRI0536 Content of Tumor Necrosis Factor Alpha in Children with Juvenile Sleroderma
Authors: I. Chyzheuskaya, A. Lyatun, L. Belyaeva, S. Chesnova
Journal: Annals of the Rheumatic Diseases (2014)

<h3>Objectives</h3> To determine the content of TNF in the serum of children with juvenile scleroderma. <h3>Methods</h3> Baseline demographics, clinical characteristics and disease activity parameters have been documented. Determination of the concentration of tumor necrosis factor alpha (TNF-α) held in the serum by ELISA using kits from Immunotech (France). <h3>Results</h3> We examined 65 children with juvenile scleroderma (JS) (mean age 12.3±3.6 years), among them 24 children with systemic sclerosis (SS) and 41 children with limited scleroderma (LS). According to the results of the study found a significant increase of TNF-α in the serum of children with JS when compared with the control group. Individual values of TNF-α in serum were elevated in 83.3% children with SS and in 65.8% children with LS. Maximum values of this index were observed in children with rapidly progressive course SS (263.98 pg/ml). TNF-α levels did not differ in patients with diffuse and limited forms of systemic sclerosis. Also there was no correlation with clinical parameter of SS, as skin score. The content of TNF-α was not correlated with patient age and disease duration. Correlation analysis revealed the dependence of the level of TNF-α on the degree of disease activity (r=0.73, P&lt;0.001). The positive relationship of TNF-α content with the content of C-reactive protein (r=0.64, P&lt;0.01). The content of TNF-α was significantly higher in patients with rheumatoid factor higher values than children with normal levels of rheumatoid factor (P&lt;0.05). <h3>Conclusions</h3> The results suggest that increasing the level of TNF-α at JS reflects inflammatory disease activity and justifies the use of inhibitors of TNF-α for the treatment of scleroderma in childhood. <h3>Acknowledgements</h3> This study would not have been possible without the collaboration of numerous Belarusian pediatric rheumatologists, patients and their parents. <h3>Disclosure of Interest</h3> None declared <h3>DOI</h3> 10.1136/annrheumdis-2014-eular.5906
Hidradenitis suppurativa: haploinsufficiency of gamma-secretase components does not affect gamma-secretase enzyme activity<i>in vitro</i>
Authors: A.E. Pink, D. Dafou, N. Desai, O. Holmes, C. Hobbs, C.H. Smith, P. Mortimer, M.A Simpson, R.C. Trembath, J.N. Barker
Journal: British Journal of Dermatology (2016)

Hidradenitis suppurativa (HS) is a chronic inflammatory dermatosis that presents with nodules, cysts, abscesses and sinus tracts in apocrine gland-bearing areas.It is thought to occur secondary to follicular occlusion, has been associated with smoking and obesity and may be inherited in an autosomal dominant manner in a minority of cases 1 .Heterozygous mutations in the gamma-
Case 20-1998
Authors: John L. Berk, Eugene J. Mark
Journal: New England Journal of Medicine (1998)

Presentation of CaseA 53-year-old man with cardiac amyloidosis was admitted to the hospital because of hemoptysis and a pulmonary lesion.The patient had first been seen at this hospital four years earlier because of atrial fibrillation, congestive heart failure, and an embolic stroke. Microscopical examination of a specimen from a right ventricular endomyocardial biopsy showed amyloid believed to be related to transthyretin (prealbumin), a finding indicative of familial amyloidosis. A coronary angiographic study revealed minimal atherosclerosis. There was moderate global and inferior hypokinesis, with severe mitral regurgitation. Symptoms were well controlled with colchicine, furosemide, warfarin, and propranolol.Twenty months . . .
AB0073 Maternal collagen-induced arthritis and co-administration of etanercept change tnf protein level in placenta and epiphyseal cartilage in fetuses
Authors: A. Korobowicz-Markiewicz, F. Burdan, J. Szumiło, R. Klepacz, J. Dudka
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Etanercept interferes with the tumor necrosis factor (TNF) and is widely used in various autoimmune diseases. However, its developmental toxicity has not been fully established. <h3>Objectives</h3> The aim of the study was to evaluate expression of gene coded TNF on the mRNA and protein level in case of the collagen-induced arthritis (CIA) with or without co-administration of the solutable TNF receptor (etanercept). <h3>Methods</h3> Female rats were immunized according to the Trentham's method. The drug (0.4 and 4.0 mg/kg) was subcutaneously injected to animals that exhibited one or higher severity score in the visual system for evaluation of CIA rodent model. After the last injection all the females were inseminated and pregnant animals were kept without any xenobiotics until gestational day 21 when cesarean section was performed. Parallel CIA, etanercept-exposed animals without CIA and untreated (sham operated) females were also examined. TNF gen expression was evaluated in placental homogenates using RNase Protection Assays. The TNF protein level was examined by ELISA and immunohistochemically in placenta and epiphyseal cartilages. <h3>Results</h3> Insignificant changes of the gen expression were found among examined groups but the results were highly dependent on the organ weight. Protein level of TNF was significantly decreased in group with CIA treated with etanercept when compared with CIA. However, TNF immunoreactivity and localization of the cytokine immunostainig in placenta and epiphyseal cartilage was similar in all examined groups. Conclusion: Unlike insignificant changes of TNF gen expression, etanercept decreased protein level of cytokine in placental and epiphyseal homogenates without additional changes in its immunoexpression. <h3>Conclusions</h3> Conclusion: Unlike insignificant changes of TNF gen expression, etanercept decreased protein level of cytokine in placental and epiphyseal homogenates without additional changes in its immunoexpression. <h3>Disclosure of Interest</h3> None Declared
ELEVATED TROPONIN AS A RISK MARKER FOR REDUCED GLOBAL LONGITUDINAL STRAIN IN HYPERTROPHIC CARDIOMYOPATHY
Authors: Anushree Agarwal, Kambiz Shetabi, Rayan Yousefzai, Saurabh Aggarwal, M. Fuad Jan, Chi Cho, Michelle Bush, Bijoy K. Khandheria, Timothy E. Paterick, A. Jamil Tajik
Journal: Journal of the American College of Cardiology (2015)
Ectopic Pregnancy in a Patient with Three Fallopian Tubes
Authors: W. Stewart Whittemore
Journal: New England Journal of Medicine (1950)

THE presence of ectopic pregnancy in a supernumerary fallopian tube is sufficiently unusual to warrant the report of a case. Novak1 states that "duplication in the form of a third tube is very rare." The more common anomalies of the tubes consist of double fimbriated extremities or diverticula occurring in the course of an otherwise normal tube.2 Ectopic pregnancies have been reported in such outpocketings and in the extra fimbriated end of the tube. Nuñez3 described a twenty-three-year-old woman with rupture during ectopic pregnancy occurring in the right fallopian tube, which, on microscopical examination, was divided throughout its length by . . .
AB1107 Hereditary autoinflammatory syndromes in brazil: A multicenter study
Authors: A.A. Jesus, E. Fujihira, M. Watase, M.T. Terreri, M.O.E. Hilario, M. Carneiro-Sampaio, C.A. Len, S.K. Oliveira, M.C. Rodrigues, R.M. Pereira, B. Bica, N.A. Silva, A. Cavalcante, R. Marini, F. Sztajnbok, M.V. Quintero, V. Ferriani, D. Moraes-Vasconcelos, C.A. Silva, J.B. Oliveira
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> The most prevalent autoinflammatory syndromes (AIS) with an identified genetic defect are: Familial Mediterranean Fever (FMF); Tumoral necrosis fator (TNF) Receptor Associated Periodic Syndrome (TRAPS); Pediatric Granulomatous Arthritis (PGA); Cryopyrin Associated Periodic Syndromes (CAPS); and Mevalonate Kinase Deficiency (MKD) <sup>1-3</sup>. <h3>Objectives</h3> The objective of this Brazilian multicenter study was to determine the prevalence of identifiable genetic defects in patients with a clinical suspicion of AIS from the five regions of the country. <h3>Methods</h3> A cross-sectional multicenter study was performed and included 102 patients from 22 Pediatric Rheumatology centers. All patients had a clinical diagnosis of one of the following disorders: CAPS, TRAPS, FMF, MKD and PGA. One of the five AIS-related genes (CIAS1, TNFRSF1A, MEFV, MVK and NOD2) was evaluated in each patient by direct DNA sequencing, based on the most probable clinical suspect. The DNA fragments were directly sequenced and all mutations detected were confirmed in a second PCR product amplification followed by sequencing. <h3>Results</h3> The clinical diagnoses of the 102 patients were: CAPS in 28 patients, TRAPS in 31, FMF in 17, MKD in 17 and PGA in 9. Of the 102 patients, 28 (27%) had a confirmed genetic diagnosis by evaluation of only one gene per patient: 6/28 (21%) CAPS patients, 7/31 (23%) TRAPS, 3/17 (18%) FMF, 4/17 (24%) MKD and 8/9 (89%) PGA. Seven (37%) of the different 19 mutations identified were novel, such as T433I and K173E (<i>CIAS1</i>), G87S and D122H (<i>TNFRSF1A</i>), A21V (<i>MVK</i>), and D512H and Y563H (<i>NOD2</i>). One TRAPS patient was homozygous for the G87S mutation. <h3>Conclusions</h3> We have found that approximately one third of the Brazilian patients with a clinical suspicion of AIS have a confirmed genetic diagnosis. <h3>References</h3> Jesus AA, Oliveira JB, Hilario MO et al. Pediatric hereditary autoinflammatory syndromes. J Pediatr (Rio J) 2010;86:353-66. Glaser RL, Goldbach-Mansky R. The spectrum of monogenic autoinflammatory syndromes: understanding disease mechanisms and use of targeted therapies. Curr Allergy Asthma Rep 2008;8:288-98. Masters SL, Simon A, Aksentijevich I, Kastner DL. Horror autoinflammaticus: the molecular pathophysiology of autoinflammatory disease. Annu Rev Immunol 2009;27:621-68. <h3>Disclosure of Interest</h3> None Declared
The Graham-Steell Murmur Re-Evaluated
Authors: Keith E. Cohn, Herbert N. Hultgren
Journal: New England Journal of Medicine (1966)

IN 1888 Graham Steell described his now famous left-sternal-border diastolic murmur and attributed its origin to pulmonary regurgitation caused by high pressure in the pulmonary artery in patients with mitral stenosis,1:In cases of mitral obstruction there is occasionally heard over the pulmonary area and below this region, for the distance of an inch or two along the left border of the sternum, and rarely over the lowest part of the bone itself, a soft blowing diastolic murmur immediately following or, more exactly, running off from the accentuated second sound, while the usual indications of aortic regurgitation afforded by . . .
S97 Is an Increased Tendency to Clot a Risk Factor For Developing Idiopathic Pulmonary Fibrosis?
Authors: V Navaratnam, A Fogarty, T McKeever, N Thompson, RG Jenkins, SR Johnson, G Dolan, M Kumaran, K Pointon, RB Hubbard
Journal: Thorax (2012)

<h3>Background</h3> The aetiology of idiopathic pulmonary fibrosis (IPF) remains poorly understood. Recent animal studies and epidemiological data have suggested that activation of the coagulation cascade in the lung may have an important role in the pathogenesis of IPF. <h3>Methods</h3> We recruited incident cases of physician diagnosed IPF from five teaching hospitals and eight district general hospitals in England and Wales. Age and sex matched general population controls were recruited from the same region. Participants were asked for details of lifetime occupational history, current or previous illnesses, medication and smoking. Each case and control then had a venous blood sample taken for a thrombophilia screen, including inherited and acquired clotting defects. We also collected high resolution computed tomography (HRCT) scans for all cases, which were reviewed by two experienced thoracic radiologists to confirm the diagnosis of IPF. After excluding individuals on warfarin, logistic regression was used to estimate odds ratios for the association between a prothrombotic state and IPF, adjusting for age, sex and highly sensitive C Reactive Protein (hsCRP). Individuals were defined as being prothrombotic if they had at least one clotting defect present. The analysis was then repeated, stratifying cases by radiological diagnosis. <h3>Results</h3> Our study included 306 incident cases of IPF(mean age at diagnosis 72.6 years, 70.6% male) and 256 controls (see Table 1). We found an increased tendency to clot among our cases (Odds Ratio [OR] 4.67; 95% Confidence Interval [CI] 3.00 to 7.23) compared to controls. After stratifying by radiological diagnosis, this association was stronger in those with definite usual interstitial pneumonia (UIP) (OR 5.86; 95% CI 3.08 to 11.15) compared to probable UIP (OR 3.47; 95% CI: 1.92 to 6.29). There was no effect modification by age, sex or hsCRP. <h3>Conclusion</h3> An increased tendency to clot appears to be an independent risk factor for developing IPF. A clinical trial using one of the new, safer anticoagulants may be warranted.
PWE-137 The role of<sup>99m</sup>technetium-labelled hepato imino diacetic acid (HIDA) in the management of biliary pain
Authors: R Dave, A Cockbain, G Toogood
Journal: Gut (2012)

<h3>Introduction</h3> Biliary pain is a common presentation in the acute surgical take and the surgical clinic. In patients with normal ultrasound findings, symptoms can sometimes be disregarded as being non-specific. We propose that in this cohort, a HIDA scan is a useful investigation, and patients with a positive test have good results following cholecystectomy. <h3>Methods</h3> We obtained reports of all HIDA scans with an abnormal ejection fraction (EF &lt;40%) performed in our centre from 15 May 2007 to 28 December 2010. This database was cross-linked with a prospectively-maintained database and electronic records of patients undergoing cholecystectomy in the same period. All patients with a positive HIDA who went on to have laparoscopic cholecystectomy (LC) were followed-up by a review of the electronic records, and a telephone interview to asses symptom improvement. <h3>Results</h3> 50 patients were investigated. Mean age was 48, and majority were female. Ultrasound findings revealed no stone disease and normal gall bladder in 96%. 92% of patients were happy with the decision to proceed with LC, and 87.5% felt that their symptoms were improved (62.5% “Very Much Improved”). Post-operatively, 56.3% had no residual pain whatsoever and 31.3% had only occasional mild discomfort. The histology was pathological in 83%; 29% had stones in the gall bladder. During the HIDA scan, injection of a CCK-analogue caused pain in 56%. Symptoms were “Very Much Improved” after LC in 74% and 44% respectively in the responders and non-responders to CCK-analogue injection. The sensitivity of CCK-analogue injection was 68% and specificity was 50%. <h3>Conclusion</h3> HIDA scan is a useful clinical tool in the diagnosis and management of patients with typical biliary pain and normal ultrasound. Outcomes following LC in this cohort of patients are favourable, with high patient satisfaction. The injection of a CCK analogue is a sensitive adjunct to the test, but non-response does not rule out benefit from LC. <h3>Competing interests</h3> None declared.
P688The effect of ionizing radiation on morphological and molecular changes of the rat myocardium
Authors: B Kura, C Viczenczova, K Frimmel, T Ravingerova, N Tribulova, L Okruhlicova, A Lazou, R Kukreja, M Fulop, J Slezak
Journal: Cardiovascular Research (2014)

One of the most widely used methods of treating oncological patients is ionizing radiation therapy. Radiation beam causes damage to the cancer cells which can reduce cancerous mass and leads to recovery of the oncological patients. On the other hand irradiation of other nearby tissues like myocardium can cause some damage which can induce serious health problems leading to the heart ischemia and heart failure.
Accumulation of Tc-99m HMDP in Bony Structures of Immature Teratoma in a Child
Authors: JUNKO TOHYAMA, SATORU OHBA, CHIKAO SUGIE, HIROYUKI OGINO, MASAKI HARA, YUTA SHIBAMOTO
Journal: Clinical Nuclear Medicine (2003)

TOHYAMA, JUNKO M.D.; OHBA, SATORU M.D.; SUGIE, CHIKAO M.D.; OGINO, HIROYUKI M.D.; HARA, MASAKI M.D.; SHIBAMOTO, YUTA M.D. Author Information