tbuckley/cabot-search huggingface dataset:
The value of preoperative axillary ultrasound staging in the management of early breast cancer.
Authors: DM O'Mahony, LM Quinn, A Hafeez, BM Dunne, M Griffin, GF Wilson, RA McDermott, TJ Boyle, EM Connolly
Journal: Cancer Research (2009)

Abstract Abstract #1023 Background: The prognosis of breast cancer is strongly associated with the presence of metastatic disease in the axillary lymph nodes at the time of diagnosis. Sentinel lymph node biopsy (SLNB) is the current standard of care for staging a clinically negative axilla in early breast cancer. Approximately 25% of women with early stage breast cancer undergoing SLNB are node positive and require completion axillary lymph node dissection (ALND). Ultrasound guided fine needle aspiration cytology (FNAC) of axillary lymph nodes is a minimally invasive technique that can be used preoperatively to stage the axilla in breast cancer patients, reducing the number of operative procedures required for staging and local control of disease. Aim: To determine the sensitivity and specificity of ultrasound guided axillary FNAC to detect positive axillary lymph nodes in breast cancer patients and to determine the number of patients who avoided unnecessary SLNB. Methods: Newly diagnosed invasive breast cancer patients were prospectively followed from January 2007 to June 2008. Patients with stage IV breast cancer, clinically node positive disease and patients who did not proceed to surgery were excluded. Criteria for a suspicious sonographic axillary node included diffuse cortical thickening &amp;gt;3mm, focal nodular cortical thickening and a mass-like appearance with loss of the fatty hilum. Results: 133 patients who met the inclusion criteria were diagnosed with invasive breast cancer between January 2007 and June 2008. Median age was 60 [21-87]. 49 patients had T1 tumours, 77 patients had T2, and 7 patients had T3 tumours. 126 (95%) patients had axillary ultrasounds, 44 ( 35%) of which showed abnormal axillary lymph nodes. 38 ( 86%) of these 44 patients proceeded to ultrasound guided axillary FNAC and 27 (71%) of these were positive for malignant cells. All patients with positive axillary nodal FNAC underwent axillary clearance and all had positive nodes on final histopathology. The median number of positive nodes was 2, range was 1 to 21. 26 (20%) patients avoided unnecessary SLNB. 82 patients had a negative axillary ultrasound and 27 of these had axillary node positive disease. The median number of positive nodes was 1, the range was 1 to 8.&amp;#x2028; &amp;#x2028; Conclusion: Ultrasound guided axillary FNAC has a high specificity and positive predictive value in radiologically suspicious nodes. A positive FNAC allows definitive treatment of the axilla in radiological node positive patients and avoids the unnecessary step of SLNB. Citation Information: Cancer Res 2009;69(2 Suppl):Abstract nr 1023.
Pharmacist-Prescribed Birth Control in Oregon and Other States
Authors: Y. Tony Yang, Katy B. Kozhimannil, Jonathan M. Snowden
Journal: JAMA (2016)

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Comfort Care for Patients Dying in the Hospital
Authors: Craig D. Blinderman, J. Andrew Billings
Journal: New England Journal of Medicine (2015)

For hospitalized patients whose death is imminent, palliative care can alleviate distressing symptoms that are common during the last few days or weeks of life. The essentials of such care that are presented in this review are intended to provide both generalists and specialists in fields other than palliative care with a practical, evidence-based approach to alleviating these symptoms in patients who are dying in a hospital. Communication skills that are essential to personalized care and goal setting are described briefly; the alleviation of the psychosocial and spiritual suffering that is often faced by terminally ill patients and their families is addressed only incidentally. The term “comfort care” is used here to describe a set of the most basic pallia tive care interventions that provide immediate relief of symptoms in a patient who is very close to death. Typically, these measures are used to achieve comfort for the patient rapidly; diagnostic or therapeutic maneuvers that might be appropriate for palliation in earlier stages of the illness are usually not considered in this context. Many elements of this approach can be used to ease patients’ distress in other phases of a life-threatening illness and in nonhospital settings, and they can also be applied to relieve symptoms in patients with less grave conditions. The Need for Comfort-Care Skills in Hospital Pr actice Although a growing proportion of deaths in the United States now occur at home or in nursing homes, hospitals remain a major site for end-of-life care; in 2010, 29% of deaths occurred in the hospital, and the average terminal admission lasted 7.9 days. 1 Multiple distressing symptoms affect hospitalized patients who have advanced, life-threatening illnesses, 2,3 and some of these symptoms worsen as the patient approaches death. 4 Poorly controlled symptoms have been documented in patients with advanced cancer, congestive heart failure, chronic obstructive pulmonary disease (COPD), and many other life-threatening conditions. 5,6 The meticulous management of distressing symptoms is important in any phase of illness, but it becomes a primary focus near the end of life. 7 Palliative care services can reduce the distress caused by symptoms and improve the quality of life of patients near the end of life. 8 However, the current scarcity of board-certified palliative care specialists — a workforce shortage that is projected to continue far into the future — means that the responsibility for ensuring excellent end-of-life care for dying patients will continue to fall primarily on generalists and on specialists in areas other than palliative care. 9,10 Thus, familiarity with basic comfort measures is an essential skill for all clinicians who are caring for patients whose death is imminent. 7,11
Abstract 2824: Therapeutic potential of multi-kinase inhibitor sorafenib in osteosarcoma cells
Authors: Yunmi Ko, Jun Ah Lee
Journal: Cancer Research (2012)

Abstract Osteosarcoma (OS) is the most common primary malignant bone tumor in childhood and adolescence. The introduction of multiagent chemotherapy has greatly improved the survival of patients with osteosarcoma, however, the improvement in survival has reached a plateau. Therefore, search for novel agents focused on different mechanisms is mandatory to further improve the survival of osteosarcoma patients. Sorafenib is the first oral multi-kinase inhibitor that directly blocks the auto-phosphorylation of several receptor tyrosine kinases (VEGFR1, 2 and 3, PDGFRα, c-Kit and RET) and inhibits Raf kinase isoforms (wild-type Raf1, and B-Raf and mutant b-raf V600E) activity to prevent tumour growth by anti-angiogenic, antiproliferative and/or pro-apoptotic effects. Here, we describe the effect of sorafenib in human OS cell lines on the proliferation and migration. And we also report combination effects with irradiation (IR) and cisplatin. We measured cell proliferation by MTT assay and used Annexin V and flow cytometry to assess whether sorafenib induce apoptosis in the OS cells. Next the migration of sorafenib-treated OS cells was determined by wound-healing assay and the synergistic effect between sorafenib and IR was evaluated using colony-forming assay. Also CI values of drug combinations of cisplatin and sorafenib in OS cells were calculated using Calcusyn software to assess whether sorafenib can be useful when used in conjunction with cisplatin. We found that sorafenib effectively inhibits cell proliferation, induced apoptosis, and prevents cellular migration. And our results demonstrate that the combination of two drugs, sorafenib and cisplatin, showed synergistic effects and colony-forming assay showed that sorafenib enhanced the radiosensitivity of OS cells. In conclusion, we found that sorafenib exerts therapeutic potentials in OS cells and suggests the possibilities of using sorafenib as a potential adjuvant therapy for the treatment of osteosarcoma. 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 2824. doi:1538-7445.AM2012-2824
P17 TIPS outcomes for Budd-Chiari: a single tertiary centre experience
Authors: J. Macnaughtan, B. Hogan, G. Tritto, M. Mullan, D. Yu, D. Thorburn, J. O'Beirne, R. Jalan, D. Patch, A. Burroughs
Journal: Gut (2011)

<h3>Introduction</h3> TIPS insertion is an important intervention in the management of Budd–Chiari syndrome. We describe the experience of a single tertiary referral centre. <h3>Aim</h3> The aims of this study were to describe the series of patients undergoing TIPS insertion for Budd–Chiari syndrome at the Royal Free Hospital, survival post-TIPS insertion and re-intervention rates. <h3>Method</h3> A retrospective analysis of the Royal Free Hospital radiology database was conducted to identify all patients who underwent all TIPS procedures between January 1991 and January 2011. Patient records were used to subsequently identify those patients in whom Budd–Chiari was the principal indication for TIPS insertion and to characterise this patient cohort. <h3>Results</h3> 1073 TIPS-related procedures were conducted at the Royal Free Hospital between January 1991 and January 2011. Of these, 51 patients underwent TIPS insertion for Budd–Chiari syndrome between January 1991 and January 2011 of which 61% (31/51) were female and 39% (20/51) were male. The mean age at the time of TIPS insertion was 40 years (±1.96). All patients were anticoagulated post procedure. 1-year transplant-free survival post-TIPS insertion was 93%. TIPS insertion could not be achieved in three patients. TIPS stenosis/occlusion was more common than in other TIPS indications. The mean number of TIPS-related interventions was 2.5 (1–10). Local thrombolysis with tissue plasminogen activator was required in three cases and patency/intervention rates were significantly improved with the addition of asprin to standard warfarin anticoagulation. No patients proceeded to liver transplantation. Regenerative nodules post TIPS were common on surveillance cross sectional imaging. <h3>Conclusion</h3> Excellent 1-year transplant-free survival can be obtained in Budd–Chiari syndrome with TIPS placement. Patients are complex and may require multiple interventions and therefore probably best managed in experienced centres.
AB0821 Analysis of organ damage in mixed connective tissue disease
Authors: M. Olesinska, Z. Czuszynska, A. Felis-Giemza, K. Walkiewicz-Pielaszek, A. Paradowska-Gorycka, L. Rutkowska-Sak, M. Marusak-Banacka, E. Wiesik-Szewczyk, Z. Zdrojewski
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Irreversible organ damage is a cause of mortality and morbidity in chronic inflammatory diseases. In most of them validated tools for disease damage assessment were prepared. There is no such a method in mixed connective tissue disease (MCTD). <h3>Objectives</h3> To estimate disease damage by prepared method in MCTD. <h3>Methods</h3> The wide range of clinical assessment of 69 MCTD patients (pts) was performed. Diagnosis was made based on Kasukawa’s criteria. For assessment of damage extend we used index (DI) prepared for the study, based on SLICC/ACR DI, involving organs and systems affected on MCTD clinical course. To each organ involvement point scoring was added. To analyze correlation of DI with demographic and clinical variables Spearman’s rank correlationwas used. Study was accepted by Local Ethics Committee. <h3>Results</h3> Median of MCTD pts’ age was 45 years (16 - 66), median of disease duration: 117,8 months (10-420). Median of DI was 3,0 (0- 12). The lowest values of DI: 0-2 were observed in 29 pts (42%), 3-6 in 31 patients (45%) and 7-10 in 7 pts (10%). The most often damage involved: skin, musculoskeletal, cardiovascular and pulmonary system. DI correlated with age of pts (R=0.426; P&lt;0.001), disease duration (R=0.492; P&lt;0.001), age at the diagnosis (R=0.296; P=0.015) and cumulative dose of corticosteroids (R=0.275; P=0.023). <h3>Conclusions</h3> Our data confirm that the damage is a great concern in MCTD. Disease damage assessed by the method prepared in the study is related to age of pts, disease duration and cumulative corticosteroids dose. <h3>Disclosure of Interest</h3> None Declared
Circadian Variation in the Frequency of Onset of Acute Myocardial Infarction
Authors: James E. Muller, Peter H. Stone, Zoltan G. Turi, John D. Rutherford, Charles A. Czeisler, Corette Parker, W. Kenneth Poole, Eugene Passamani, Robert Roberts, Thomas Robertson, Burton E. Sobel, James T. Willerson, Eugene Braunwald
Journal: New England Journal of Medicine (1985)

To determine whether the onset of myocardial infarction occurs randomly throughout the day, we analyzed the time of onset of pain in 2999 patients admitted with myocardial infarction. A marked circadian rhythm in the frequency of onset was detected, with a peak from 6 a.m. to noon (P<0.01). In 703 of the patients, the time of the first elevation in the plasma creatine kinase MB (CK-MB) level could be used to time the onset of myocardial infarction objectively. CK-MB—estimated timing confirmed the existence of a circadian rhythm, with a threefold increase in the frequency of onset of myocardial infarction at peak (9 a.m.) as compared with trough (11 p.m.) periods. The circadian rhythm was not detected in patients receiving beta-adrenergic blocking agents before myocardial infarction but was present in those not receiving such therapy. If coronary arteries become vulnerable to occlusion when the intima covering an atherosclerotic plaque is disrupted, the circadian timing of myocardial infarction may result from a variation in the tendency to thrombosis. If the rhythmic processes that drive the circadian rhythm of myocardial-infarction onset can be identified, their modification may delay or prevent the occurrence of infarction. (N Engl J Med 1985; 313:1315–22.)
AB0117 NK cells isolated from synovial fluid amplify the inflammatory response of fibroblast-like synoviocytes
Authors: A. Scanu, F. Oliviero, D. Mavilio, P. Sfriso, L. Punzi
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Natural killer (NK) cells represent one of the major components of innate immune system and are very important in both early and chronic phases of inflammatory responses. NK cells might contribute to the disease onset through the release of great amount of pro-inflammatory cytokines and through a direct cytolitic activity. However, the role of NK cells in joint inflammation remains unclear. <h3>Objectives</h3> To determine whether NK cells are present in synovial fluid (SF) and whether they might play a role in amplifying the inflammatory process. <h3>Methods</h3> Mononuclear cells were isolated by density gradient centrifugation from SF collected by arthrocentesis from the knees of 4 untreated patients with inflammatory arthritis (3 seronegative spondiloarthritis and 1 psoriatic arthritis). NK cells were isolated from mononuclear cells by negative immunomagnetic selection. Human fibroblast-like synoviocytes (FLS) were obtained by synovial tissue explants from patients with OA and cocultured for 24 h at 10×10<sup>3</sup> cells/well in 96-well plates with increasing ratios of NK cells (1:1; 1:2; 1:5; 1:10; 1:20). FLS or NK cells were cultured alone as control. Culture supernatants were tested by ELISA for the production of IL-1β, IL-8, CCL2 and TGFβ1. <h3>Results</h3> NK cells were isolated from all 4 SF collected. The percentage of NK cells in mononuclear cells was 0.14 in SF1, 0.16 in SF2, 1.06 in SF3 and 0.56 in SF4. IL-1β and TGFβ1 were not detectable in all culture supernatants. When FLS were cocultured with NK cells the production of IL-8 and CCL2 increased in a NK ratio-dependent manner. FLS or NK alone did not release significant levels of IL-8 and CCL2. <h3>Conclusions</h3> This study confirms that NK cells are also present in synovial fluid and they might potentially contribute to amplification of the inflammatory process within the joint. The increased cytokine production might be due to the capacity of NK cells to produce fibroblast-activating factors or to direct interactions with synovial cells. <h3>Disclosure of Interest</h3> None Declared
SP0201 Autoantibodies in hypertensive disease of pregnancy
Authors: F. Herse
Journal: Annals of the Rheumatic Diseases (2013)

One of the leading causes for maternal and perinatal morbidity and mortality in pregnancy is preeclampsia. Preeclampsia is defined as an increase in blood pressure (&gt;140/90 mmHg) appearing after 20 weeks of gestation and proteinuria (&gt;300 mg/l) in a previously normotensive woman. It is a major healthcare problem, affecting 5–7% of pregnant women worldwide and mothers and children suffer from an increased long-term cardiovascular risk. Nonetheless, the underlying molecular mechanisms remain unclear, immunological mechanisms and the renin–angiotensin system have been implicated in the development of these pregnancy disorder. Agonistic autoantibodies to the angiotensin II receptor type I (AT1-AA) have been identified in preeclamptic mothers and fetus. This observation unified the two hypothesis he epitope is located on the second extracellular loop of the AT1-receptor. AT1-AA induce signal transduction including the protein kinase C, the mitogen-activated protein pathway and activate the transcription factors NF-kB and AP-1. AT1-AA have been found in various rat models of preeclampsia. These data indicate that the generation of AT1-AA may be secondary to placental ischemia, vascular damage, and enhanced inflammatory response. Passive transfer of AT1-AA to pregnant rodents induce a preeclamptic phenotype and an angiotensin II sensitivity which also appears in the human situation. The data support the hypothesis that preeclampsia is an autoimmune disease in which key features of the disease result from autoantibody-induced angiotensin receptor activation. This hypothesis has implications regarding preeclampsia screening, diagnosis and therapy. However, future studies are warranted to confirm this hypothesis. <h3>Disclosure of Interest</h3> None Declared
THU0489 Antibodies Binding to DRP-4 and Macropain Subunit C2 as a Potential Marker of AOSD
Authors: M. Hoepfner, T. Witte, N. Pursche, F. Moosig, W. Gross, R. E. Schmidt, N. T. Baerlecken
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Making the diagnosis of adult-onset Still's disease (AOSD) is mainly based on the exclusion of inflammatory, infectious and malignant diseases. There are no specific clinical or laboratory findings for AOSD. Elevated ferritin levels, liver enzyme levels, C-reactive protein levels, erythrocyte sedimentation rate and leukocytosis can be found in other inflammatory diseases as well. <h3>Objectives</h3> We aimed to identify new autoantibodies as diagnostic tools for AOSD. <h3>Methods</h3> We were studying sera of 3 patients with AOSD using a protein array loaded with more than 27000 human recombinant proteins (imagenes biolifesciences, Berlin). Sera of patients with SpA, RA, eGPA, GPA, HIV infection, B-NHL, CRPS, GCA, PMR, MS, osteoarthritis, TA and sarcoidosis served as controls. In the further process, we established an ELISA against a new autoantigen identified by the array in order to measure the autoantibodies in larger patient numbers. <h3>Results</h3> Using the protein array, we detected IgG autoantibodies binding to Dihydropyrimidinase-related protein 4 (DRP-4) (collapsin response mediator protein 3) and in 2/3 patients with AOSD IgG autoantibodies binding to proteasome subunit alpha type-1 (EC 3.4.25.1) (proteasome component C2) (macropain subunit C2) (multicatalytic endopeptidase complex subunit C2) in 2/3 AOSD patients, but not in more than 50 controls. Using the ELISA, we detected Auto-Abs binding to Macropain subunit C2 and DRP-4 in 65% of the patients with AOSD, in 0.7 % of blood donors, 9.1% of RA patients with RA, 10% of GPA patients, 22% of the patients with PMR and GCA, 3.4% of the patients with Sjögren's syndrome, 10.5% of the SLE patients, 21% of the patients with febrile severe infections and in 0.7% of the patients with malignant diseases. <h3>Conclusions</h3> Autoantibodies against DRP-4 and Macropain C2 are associated with AOSD and may be useful as a diagnostic tool of AOSD. <h3>Disclosure of Interest</h3> None Declared
P38 Homodynamic effects of prolonged treatment with midodrine in non-azotemic pre-ascitic, ascitic and refractory ascites cirrhotic patients
Authors: H. Badran, A. Moaty, A. A. Basuni, W. F. A. Aziz, E. A. Rewisha, I. A. Waked
Journal: Gut (2011)

<h3>Introduction</h3> Splanchnic arterial vasodilatation has related to hyperdynamic circulation and impaired natriuresis in advanced cirrhosis and was suggested to be responsible for the subtle sodium retention in pre-ascitic cirrhosis. α Adrenergic agonist may reverse this condition. <h3>Aim</h3> This study aimed to evaluate the effects of treatment with the α1-adrenergic agonist midodrine on systemic haemodynamics in non-azotemic cirrhotic patients. <h3>Method</h3> 154 cirrhotic patients were studied. The patients were classified into: absent ascites, mild to moderate diuretic responsive ascites and refractory ascites. Patients were randomly selected to receive either oral midodrine 10 mg, three times a day or placebo The following parameters were assessed for all patients: mean arterial pressure (MAP), cardiac output (CO), plasma rennin (Pl R) and renal resistive index (RRI) at baseline, 7 days after administration of oral midodrine 10 mg, three times daily, and 3 months after administration of oral midodrine 2.5 mg, three times a day. <h3>Results</h3> Midodrine administration induced a significant increase in MAP mention levels and P and significant decreases in CO mention levels and P in patients without and with mild to moderate ascites but not in patients with refractory ascites. As well as significant decreases in Pl R activity mention levels and P and RRI in patients without and with mild to moderate ascites but not in patients with refractory ascites <h3>Conclusion</h3> The administration of midodrine improves systemic haemodynamics associated with a suppression of the renin activity in cirrhotic patients without or with mild ascites. But had no effect in patients with refractory ascites