tbuckley/cabot-search huggingface dataset:
The Good Life
Authors: Steven H. Woolf, Jason Q. Purnell
Journal: JAMA (2016)

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P144 Case Series: Choosing Thrombolysis in Acute Pulmonary Embolism (PE) – Massiveness or Instability?
Authors: B Khan, R Lee, HA Raouf
Journal: Thorax (2012)

<h3>Background</h3> PE has significant mortality risk particularly in “PE with haemodynamic instability” or “massive PE” where blood pressure, attributable to PE, is sustained below 90mmHg.<sup>[1,2]</sup> Thrombolysis in this patient group is associated with reduced mortality and faster restoration of lung perfusion with approval by NICE <sup>[1,2]</sup> Another important group of patients with apparent haemodynamic stability but documented right ventricular (RV) compromise or myocardial injury (e.g. echocardiogram evidence of RV strain or raised Troponin) is recognised (“sub-massive” PE) where considerable debate remains as to reliable prognostication and appropriateness of thrombolysis. <h3>Aims</h3> Recognising a tendency in our district general hospital to treat PE aggressively, we sought to assess our own practise with regards to thrombolytic therapy in PE to better understand our interpretation of NICE guidance and the wider literature. <h3>Objective</h3> Assess routine quantification of haemodynamic instability of the acutely unwell patient in the clinical environment and the extent with which knowledge of right ventricular compromise and cardiac biomarkers influenced decision to thrombolyse. <h3>Methods</h3> Retrospective review of case records. Data was extracted from the medical records by one of the authors followed by joint scrutiny by all authors. <h3>Results</h3> From June 2010 over 24 months, 17 patients (6 males, 11 females) have been thrombolysed. Median age 62 (range 24–90). Of these one patient died 4 days later of sepsis and multi organ failure, and one developed a haematoma in her arm which resolved with conservative management. Of these patients only two Massive i.e. haemodynamically unstable with one thrombolysed on the ITU. In the submassive PEs, supporting evidence for thrombolysis was CT in 5 cases, and echo 5, both in 2, and lab (troponin rise) in 9 cases. <h3>Conclusion</h3> Thrombolysis in PE especially in submassive PEs remains an area of controversy and clinically a dilemma at times. Our case series shows that patient selection supported by relevant investigations, appropriate patients can benefit without any untoward events. <h3>References</h3> NICE CG144 Venous thromboembolic diseases: full guideline. Jaff MR et al. Management of massive and submassive pulmonary embolism, iliofemoral deep vein thrombosis, and chronic thromboembolic pulmonary hypertension: a scientific statement from the American Heart Association. Circulation 2011.
Abstract LB-28: Regulation of FOXM1 by NADPH oxidases in malignant mesothelioma cells
Authors: Kheng Newick, Brooke Mossman, Jedd Hillegass, Stacie Beuschel, Arti Shukla, Jack Arbiser, Harvey Pass, Nicholas Heintz
Journal: Cancer Research (2010)

Abstract Malignant mesothelioma (MM) is linked to the occupational exposure to asbestos with an estimated median survival of less than two years; effective therapy is lacking. Due to long latency periods, incidence is expected to rise in regions where asbestos use has been banned, as well as where worker protection is lacking. MM cells exhibit changes in oxidant and energy metabolism, with elevated expression of the NADPH oxidase NOX4. We hypothesize that NOX4 produces reactive oxygen species (ROS) that promote uncontrolled growth through redox-dependent signaling to core cell cycle factors such as FOXM1 and FOXO3a, transcription factors involved in responses in oxidative stress and cell cycle progression. Targeted microarrays were used to assess the expression levels of 96 genes involving redox metabolism in four human MM cell lines and one control mesothelial line (LP9) immortalized with hTERT. Gene expression profiles from MM cell lines indicate tumorigenesis commonly results in elevated expression of NOX activity and adaptation to constitutive production of ROS, including up-regulation of antioxidant enzymes and cytoprotective factors. mRNA for FOXM1, a transcription factor that regulates the G2/M transition in the cell cycle, was up-regulated in all four MM cell lines, and FOXM1 continued to be expressed in MM cells, but not LP9 cells, in the absence of growth factors. Inhibitors of NOX activity markedly reduced expression of FOXM1, which correlated with dose-dependent effects on MM cell proliferation and viability. In the HM MM cell line, thiostrepton (TS), a thiazole antibiotic that inhibits the expression of FOXM1 via an unknown mechanism, increased the rate of oxidation of DCF, hyper-activated ERK1/2, and showed dose-dependent effects on MM cell viability in vitro and MM tumor growth in Fox Chase SCID mice. N-acetyl-L-cysteine blocked activation of ERK1/2 and cell death by TS, indicating the cytotoxic effects of TS in MM cells may be dependent on induction of intolerable levels of oxidative stress. In support of this possibility, inhibitors of p38 MAPK accentuated the cytotoxic effects of TS on cell viability. Our studies indicate that altered oxidant metabolism that supports expression of cell cycle factors such as FOXM1 is a common property of MM cells, and suggest that either inhibiting or accentuating the production of ROS in MM cells may be useful therapeutic approaches in the treatment of MM. Note: This abstract was not presented at the AACR 101st Annual Meeting 2010 because the presenter was unable to attend. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr LB-28.
Abstract 5106: Autophagy in malignant melanoma and breast carcinoma
Authors: Rossitza Lazova, Vincent Klump, Summar Siddiqui, Robert Camp, John Pawelek
Journal: Cancer Research (2010)

Abstract We show here for the first time that autophagy is a remarkably common characteristic of malignant melanomas and breast carcinomas and is highly associated with metastasis and poor patient outcome. Autophagy is a cytoplasmic degradative process that in cancer can provide an energy source in times of nutrient deprivation. Interest in autophagy and cancer progression has increased markedly in recent years with reports that autophagy can be both a positive and negative survival factor for cancer cells. PURPOSE. The purpose of this study was to evaluate the prevalence of autophagy in melanoma and breast carcinoma, cancers from tissues of dissimilar lineages and functions. METHODS. Standard biopsies and tumor tissue microarrays containing core samples of melanoma (n = 342 cases) or breast carcinoma (n = 611 cases) were stained by immunohistochemistry for the autophagosome marker LC3B (microtuble-associated protein light chain 3B, detected with anti-LC3B polyclonal antibody ab48394, Abcam, Inc., Santa Cruz, CA). Autophagy was verified by the LC3B granular staining pattern and, in melanoma, by electron microscopy. RESULTS. In standard biopsies of melanoma, autophagic tumor cells emerged sporadically within the in situ tumor and were apparently the source of invasive cells in the dermis. For melanoma microarrays, 82% (107/130) of primary invasive melanomas and 90% (189/212) of lymph node metastases showed nearly uniform expression of autophagy with metastases showing increased LC3B staining intensity compared to primary tumors (p &amp;lt; 0.0001). Similar results were obtained for breast carcinoma microarrays where 73% (447/611) of primary tumors showed high levels of autophagy and this correlated with poor patient outcome (p &amp;lt; 0.001). Thus autophagy appears to be a constitutive metabolic state for a majority of malignant melanomas and breast carcinomas. The diverse origins and functions of these cells suggests that autophagy may be prevalent in other malignancies as well. Thus therapies targeting autophagy should be considered as a means to deprive cancer cells of an important energy source. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 5106.
SAT0474 Differences of clinical and ultrasound (US) remission in rheumatoid arthritis (RA) depend on the stringency of the us methodology
Authors: M. Gärtner, H. Radner, G. Supp, D. Aletaha, K. Machold, J. Smolen
Journal: Annals of the Rheumatic Diseases (2013)

Background Progression of joint damage in RA occurs primarily in joints that are clinically swollen, and repair is seen only in joints with no clinical swelling.1;2 On the other hand, joints exhibiting US but not clinical swelling may progress radiologically despite clinical remission.3 This discrepancy requires elucidation to understand the value of clinical compared with US joint assessment, since except for histology, there is no true gold standard for US joint activity. Objectives To evaluate the differences in number of clinically and US active joints in RA, with special regards to the impact of US definitions of activity. Methods We performed US imaging of 22 joints of the hands of RA patients in clinical remission (CDAI≤2.8). Each joint was assessed for grey scale synovial hypertrophy (GSSH; 0=no hypertrophy; 1=hypertrophy) and power Doppler (PD) signal (0= no hyperaemia, 1= mild, 2=moderate, 3=marked). We investigated the sensitivity and specificity of clinically swollen joints (SJC) for presence of US changes and repeated this analysis using different cut points and combinations of US definitions. We further assessed changes of CDAI if clinical SJC were replaced by US active joints. Results Of the 58 patients in clinical remission, 96.6% had GSSH and 93.1% had positive PD signals. The sensitivity and specificity of clinical SJC for any US abnormality (GSSH>0 or PD>0) was 1.7% and 100%, respectively. When we used more stringent definitions of US activity (GSSH>0 & PD=3), these values changed to 22.2% and 99%. Replacing clinical by US counts in the calculation of CDAI, the US CDAI values approached the clinical CDAI with increasing stringency of the definition used (Fig.). In fact, the most stringent definition (GSSH>0 & PD=3) revealed identical average values as seen in the clinical CDAI. ![Figure][1]</img> Conclusions Low PD signals increase the numbers of patients classified as having active joints and lead to a poor sensitivity of clinical assessment in comparison to US assessment. When the PD signal is combined with assessment of GSSH, or the strength of the PD signal is considered, the differences decrease, particularly when looking at their impact on composite indices. The relevance of this finding will have to be tested in relation to radiographic progression of joint damage. 1. Klarenbeek NB et al. ARD 2010; 69(12):2107-2113. 2. Lukas C et al. ARD 2010; 69(5):851-855. 3. Brown AK et al. Arthritis Rheum 2008; 58(10):2958-2967. Disclosure of Interest None Declared [1]: pending:yes
Points: Health surveillance of preschool children
Authors: D J Lane
Journal: BMJ (1986)

August, p 395) make an important point which deserves highlighting.Fracture dislocation of the cervical spine complicating near drowning is a rare event in Britain but is seen more commonly in Australia, where body surfing is a popular sport.The advice given to rescuers in Britain is that any unconscious patient found in standing depth water should be handled as though he or she had suffered fracture dislocation of the neck.It is possible on occasions to ventilate adequately without extending the neck, but if this is not the case then the rescuer has no alternative but to tilt the head back.
PROGNOSTIC PLAQUE BIOMARKERS FOR THE RISK STRATIFICATION IN PERIPHERAL VASCULAR DISEASE
Authors: Tobias Koppara, Fumiyuki Otsuka, Lawrence Garcia, Xiaoqing Zhao, Kazuyuki Yahagi, Oscar Sanchez, Hiroyoshi Mori, Michael Joner, Frank Kolodgie, Renu Virmani
Journal: Journal of the American College of Cardiology (2015)
Abstract P1-05-22: Breast cancer cells that undergo an Epithelial-to-Mesenchymal transition co-opt LPP, a regulator of mesenchymal cell migration and invasion.
Authors: E Ngan, JJ Northey, J Ursini-Siegel, PM Siegel
Journal: Cancer Research (2012)

Abstract Transforming Growth Factor β (TGFβ) promotes breast cancer cell metastasis to multiple sites, including the bone and lungs. TGFβ is a strong inducer of Epithelial-to-Mesenchymal transitions (EMT) and breast cancers that exhibit features of an EMT acquire stem cell-like characteristics, are highly aggressive, are resistant to therapy and are refractory to tumor suppressive processes. While TGFβ itself is non-oncogenic, it is a potent modifier of the malignant phenotype in breast cancer and is capable of enhancing the migration, invasion and metastasis of ErbB2 expressing breast cancer cells. We have identified Lipoma Preferred Partner (LPP) as an indispensable regulator of TGFβ-induced migration and invasion of ErbB2 expressing breast cancer cells. LPP is ubiquitously expressed in smooth muscle cells where it mediates cell adhesion, migration and the formation of lamellipodial extensions. We hypothesize that breast cancer cells capable of undergoing an EMT can utilize novel mediators that are engaged in promoting the migration and invasion of mesenchymal cells. We propose that LPP is one such example, which promotes the migration and invasion of ErbB2 expressing breast cancer cells that have undergone a TGFβ-induced EMT. We demonstrate that ErbB2 expressing breast cancer cells display significant increases in cell migration and invasion upon TGFβ stimulation, and such responses are dependent on LPP expression. We show that LPP re-localizes to focal adhesion complexes following TGFβ-induced EMT and it is a critical determinant in focal adhesion turnover. Furthermore, we determined that LPP targeting to focal adhesions through its LIM1 domain requires the cooperation of ErbB2 and TGFβ signaling pathways. Finally, we demonstrate that LPP promotes TGFβ-induced migration and invasion of ErbB2 expressing breast cancer cells through recruitment of α-Actinin, an actin cross-linking protein. Overall, we have identified LPP as a novel mediator that integrates TGFβ and ErbB2 signaling to promote the migration and invasion of breast cancer cells that undergo an EMT. Our data reveal that breast cancer cells, which can transition from an epithelial to mesenchymal phenotype, can engage a regulator of mesenchymal cell migration and invasion. Citation Information: Cancer Res 2012;72(24 Suppl):Abstract nr P1-05-22.
Development of a new oncology quality metric: The rate of evidence-based adherence.
Authors: Kerin Adelson, Randall F. Holcombe
Journal: Journal of Clinical Oncology (2013)

84 Background: The degree to which electronic health records enhance the quality of patient care depends on how the system is used to monitor and improve practice. In planning the transition to Epic’s electronic chemotherapy ordering platform, we saw an opportunity to increase evidence-based practice. Methods: Our Chemotherapy Council vetted more than 600 electronic protocols based entirely on published clinical trials and NCCN guidelines; modifications made to these protocols represent a divergence from clinical evidence. We examined the number of times the chemotherapy section of a protocol was modified before the first cycle to avoid counting dose modifications made for toxicities. To get the rate for the cancer center we calculated the # of discrete times all protocols were used (denominator) and the number of times all protocols were modified (numerator). We subtracted the ratio from 1 to reflect the proportion of protocols that were not modified. This ratio serves as a new quality metric – the Rate of Evidence-Based Adherence (REBA). REBA institution = 1 - Total # of modifications prior to first cycle for each protocol. The total # of uses of all protocols. Additionally, REBA can be used to examine disease group rates (REBA group ), individual provider rates (REBA provider ) and rates for individual protocols (REBA protocol ). Institutions that have implemented evidence-based clinical pathways have strived for 80% (.80) adherence. We set this as our REBA benchmark. Results: The REBA institution was .86, higher than our pre-defined goal (p&lt;0.001). There was wide variation in the REBA group (range 0.50-0.95). The REBA protocol identified two protocols (rates of .33 and .42 respectively) that were dose reduced the majority of the time. In the example of our Breast Group, the REBA provider , ranged from (.78 to .97) reflecting differing practice among 4 physicians. Conclusions: The REBA can identify faculty and disease groups who underutilize clinical evidence, facilitating feedback for quality improvement. The REBA protocol is a useful tool to identify specific chemotherapy templates that may need modification. The REBA is a powerful electronic tool, which can be utilized to monitor and enhance the rate of evidence-based practice in oncology.
P296 VITAMIN E MODULATES INFLAMMATION AND LIPID PEROXIDATION THROUGH CERAMIDE AND EICOSANOID PATHWAYS – NOVEL LIPIDOMIC INSIGHTS INTO POTENTIAL MECHANISMS OF ACTION OF VITAMIN E IN NASH
Authors: T. Pacana, V. Patel, F. Mirshahi, H.-K. Min, M. Seneshaw, R. Kaitinen, P. Puri
Journal: Journal of Hepatology (2014)
Investigating an outbreak of Clostridium perfringens gastroenteritis in a school using smartphone technology, London, March 2013
Authors: B Simone, C Atchison, B Ruiz, P Greenop, J Dave, D Ready, H Maguire, B Walsh, S Anderson
Journal: Eurosurveillance (2014)

Binary file ES_Abstracts_Final_ECDC.txt matches
Respiratory Syncytial Viral Infection in Infants with Congenital Heart Disease
Authors: Noni E. MacDonald, Caroline Breese Hall, Stephen C. Suffin, Chloe Alexson, Peter J. Harris, James A. Manning
Journal: New England Journal of Medicine (1982)

Occasional reports have suggested that infants with congenital heart disease may have an increased risk of severe illness from respiratory syncytial virus (RSV) infection. We prospectively studied 699 infants hospitalized during the winters of 1976 through 1980, when RSV was prevalent in the community; 229 of these infants had proved RSV infections acquired either before admission or during hospitalization; 27 had both congenital heart disease and RSV infection, and 46 had congenital heart disease without RSV infection. Infected infants with congenital heart disease had significantly more severe illness than those without congenital heart disease, as judged by the requirement for intensive care and assisted ventilation and by the mortality rate (37 per cent vs. 1.5 per cent, P less than 0.01). The infection was acquired nosocomially by 21 per cent of infected infants; the mortality rate from nosocomial infection was also higher in infants with congenital heart disease (44 per cent vs. 5 per cent, P less than 0.01). Pulmonary hypertension was the one condition particularly associated with severe RSV illness. Eight of the 11 infants (73 per cent) with congenital heart disease and pulmonary hypertension died during their RSV illness. The courses in infants with congenital heart disease with and without RSV infection were also compared. Their ages, types of cardiac lesions, and incidence of pulmonary hypertension were similar, but the infants with RSV infection had a higher mortality rate (37 per cent vs. 6.5 per cent, P less than 0.1).
Immunotherapy following high-dose chemotherapy (HDCT) and peripheral blood progenitor cell transplantation (PBPCT) in the treatment of high-risk early breast cancer (HREBC) and metastatic breast cancer (MBC).
Authors: F Recchia, G Candeloro, S Necozione, M Sureda, A Brugarolas, S Rea
Journal: Cancer Research (2009)

Abstract Abstract #2159 Background: Meta-analyses have shown that HDCT with PBPCT is not superior to standard dose chemotherapy in the treatment of high risk early breast cancer (HREBC) and metastatic breast cancer (MBC). The reason for the limited efficacy is due to failure to eradicate all cancer stem cells, resistant to chemotherapy, and capable to reproduce the tumor in immunodeficient mice. Lymphopenia has been described after HDCT. We have previously shown that low dose inteterleukin 2 (IL-2) and oral 13-cis- retinoic acid (RA) improved lymphocyte (L) count, and decreased vascular endothelial growth factor (VEGF), of patients with advanced tumors having a clinical benefit from chemotherapy. Primary endpoint of this study was to verify if IL-2 and RA, improving L count, and decreasing VEGF after HDCT with PBPCT of patients with advanced breast cancer, reduced angiogenic switch. Secondary endpoints were the evaluation of progression-free survival (PFS) and overall survival (OS).&amp;#x2028; Methods: From 02-1998 to 02-2003, 30 patients with HREBC and 18 with MBC were entered into the study. One month after HDCT, patients received, for 1 year, 5 days/week, 3 weeks/month, subcutaneous IL-2 (1.8 x 106 IU daily) plus RA (0.5 mg/kg body weight). Immunotherapy was continued, with intermittent schedules, up to 5 years. Patients with estrogen receptor positive (ER+) tumors received hormonal therapy, while those in premenopause received also a LHRH analogue for 5 years.&amp;#x2028; Results: Characteristics of HREBC patients: median age, 48 years (range 34-60); median number of positive axillary nodes, 13 (range-11-27); ER+/ER-: 20/10; characteristics of MBC patients: median age, 46 years (range 28-60); median number of disease sites 1.5, (range-1-4); ER+/ER-: 5/13; Major adverse effects from IL-2 were fever, rash and autoimmune reactions; no treatment-related mortality was seen. After a median follow-up of 61 months, a statistically significant improvement of L and decrease of VEGF were observed for both HREBC and MBC. 5 years PFS and OS rate were, for HREBC 76% and 85%, respectively, for MBC, 22% and 35%, respectively.&amp;#x2028; Conclusions: These data show that IL-2 administration after HDCT and PBPCT is feasible, has a moderate toxicity, gives a statistically significant improvement of L a decrease of VEGF, and seems to give an improvement of expected PFS and OS, both in HREBC and MBC. Citation Information: Cancer Res 2009;69(2 Suppl):Abstract nr 2159.
Prognostic Evaluation of Clinically Stable Febrile Neutropenia: Prospective Data from 921 Patients from the Finite Study
Authors: P.J. Fonseca, A. Carmona-Bayonas, C. Font, M. Antonio Rebollo, A. Ramchandani, J. Hernando Cubero, J. Espinosa, E.M. De Castro, I. Ghanem, J. Martínez, C. Beato, J. Virizuela, A. Blasco, Y. Bonilla, A. Manzano, E. Castañon, E. Sevillano, M.A. Vicente Conesa, F.A. De La Peña
Journal: Annals of Oncology (2014)