tbuckley/cabot-search huggingface dataset:
Pulmonary-Artery versus Central Venous Catheter to Guide Treatment of Acute Lung Injury
Authors: Arthur P Wheeler, Gordon R Bernard, B Taylor Thompson, David Schoenfeld, Herbert P Wiedemann, Ben deBoisblanc, Alfred F Connors, R Duncan Hite, Andrea L Harabin
Journal: New England Journal of Medicine (2006)

The balance between the benefits and the risks of pulmonary-artery catheters (PACs) has not been established.We evaluated the relationship of benefits and risks of PACs in 1000 patients with established acute lung injury in a randomized trial comparing hemodynamic management guided by a PAC with hemodynamic management guided by a central venous catheter (CVC) using an explicit management protocol. Mortality during the first 60 days before discharge home was the primary outcome.The groups had similar baseline characteristics. The rates of death during the first 60 days before discharge home were similar in the PAC and CVC groups (27.4 percent and 26.3 percent, respectively; P=0.69; absolute difference, 1.1 percent; 95 percent confidence interval, -4.4 to 6.6 percent), as were the mean (+/-SE) numbers of both ventilator-free days (13.2+/-0.5 and 13.5+/-0.5; P=0.58) and days not spent in the intensive care unit (12.0+/-0.4 and 12.5+/-0.5; P=0.40) to day 28. PAC-guided therapy did not improve these measures for patients in shock at the time of enrollment. There were no significant differences between groups in lung or kidney function, rates of hypotension, ventilator settings, or use of dialysis or vasopressors. Approximately 90 percent of protocol instructions were followed in both groups, with a 1 percent rate of crossover from CVC- to PAC-guided therapy. Fluid balance was similar in the two groups, as was the proportion of instructions given for fluid and diuretics. Dobutamine use was uncommon. The PAC group had approximately twice as many catheter-related complications (predominantly arrhythmias).PAC-guided therapy did not improve survival or organ function but was associated with more complications than CVC-guided therapy. These results, when considered with those of previous studies, suggest that the PAC should not be routinely used for the management of acute lung injury. (ClinicalTrials.gov number, NCT00281268.).
Abstract 4492: Colorectal cancer survival by molecular subtypes in a population-based cohort of older women
Authors: Robert Alan Vierkant, Lori S. Tillmans, Alice H. Wang, Niloy Jewel Samadder, Daniel J. Weisenberger, Peter W. Laird, Charles F. Lynch, Kristin E. Anderson, Amy J. French, Robert W. Haile, Lisa J. Harnack, John D. Potter, Susan L. Slager, Thomas C. Smyrk, Stephen N. Thibodeau, James R. Cerhan, Paul J. Limburg
Journal: Cancer Research (2012)

Abstract Background: Despite recent advances in prevention and therapy, colorectal cancer (CRC) continues to account for nearly 50,000 deaths per year in the US. TNM stage is the current CRC prognostic standard, yet within-stage prognostic heterogeneity is well documented. Microsatellite instability (MSI), CpG island methylation phenotype (CIMP), and BRAF- and KRAS-mutation status represent candidate prognostic markers. However, associations between these markers and CRC survival have not been described in a population-based setting. Methods: Data and tissue resources were obtained from the Iowa Women's Health Study (IWHS), which recruited 41,836 women, ages 55-69 years, at study entry (1986). Incident CRC cases were ascertained by annual linkage with the Iowa Cancer Registry. Archived, paraffin-embedded tissue specimens were collected from 732 representative CRC cases diagnosed through 12/31/2002. Established laboratory methods were used to characterize CRC cases: MSI-H or MSS/MSI-L (by instability in β3 vs. &amp;lt;3 out of 10 markers, respectively); CIMP+ or CIMP− (by promoter hypermethylation in β3 vs. 0-2 out of 5 genes, respectively); BRAFwt or BRAFmut (by fluorescent allele specific PCR to detect the V600E point mutation in exon 15); and KRASwt or KRASmut (by direct sequence analysis of codons 12 and 13 in exon 2). Cox regression models were fit to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for time to death of any cause adjusted for age, stage, grade, and treatment status. Results: CRC cases with informative molecular marker data ranged from 515/732 (70%) for KRAS to 548/732 (75%) for MSI status. Mean follow-up was 4.4 years for deceased individuals and 11.2 years for women alive at last contact. After multivariable adjustment, both MSS/MSI-L (p=0.004) and KRASmut (p=0.048) tumors were associated with poorer survival. Survival did not significantly differ across levels of CIMP and BRAF status. Conclusions: MSI and KRAS status may influence CRC survival among older women. 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 4492. doi:1538-7445.AM2012-4492
OP0179 Smoking as a Risk Factor for the Severity of Rheumatoid Arthritis
Authors: D. De Rooy, J. Van Nies, M. Andersson, K. Forslind, D. van der Heijde, T. Huizinga, P. Gregersen, B. Svensson, A. van der Helm-van Mil
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Smoking has been implicated as a risk factor for the development of Rheumatoid Arthritis (RA), especially for the ACPA-positive subgroup. Whether smoking also affects the severity of RA is less clear as both positive and negative studies have been published. <h3>Objectives</h3> We aimed to study the effect of smoking on the progression of joint destruction by evaluating several longitudinal cohorts. <h3>Methods</h3> Smoking status was assessed in total in 2766 patients with on average 3 radiographs: 703 RA-patients (3,656 X-rays) included in the Leiden Early Arthritis clinic, in 839 patients (2,870 X-rays) included in the Swedish BARFOT-study, in 339 patients (1,062 X-rays) from Wichita (US) and in 885 patients (885 X-rays) from the National Databank of Rheumatic Diseases. In the Dutch and Swedish patients, data on present, past and never smoking were available. In the North American patients, presence versus absence of smoking was assessed. All X-rays were scored according to the Sharp-van der Heijde Score (SHS). The majority of patients were recruited in an era when early, aggressive treatment was still uncommon. The association between smoking and the progression of joint destruction was analyzed using a multivariate normal regression analysis with the radiographic score as response variable for the patients with repeated measurements available and using a linear regression analysis for the patients with a single time-point measurement. All analyses were adjusted for age, gender and treatment. An inverse variance random effects combined analysis was performed using STATA. <h3>Results</h3> When comparing radiological joint damage for RA-patients that were never, past and current smokers, smoking was associated with a more severe disease course in the Dutch (p=0.042) and Swedish (p=0.022) patients. In the two North American cohorts, no significant associations were found between smoking and joint damage. A combined analysis showed a significant effect of smoking on joint damage (p=0.021). With regards to the risk of development of RA, it is known that smoking in particular predisposes to the development of ACPA and that these antibodies are associated with RA. The subsequent question was to what extent ACPA mediates also the association between smoking and joint damage. Therefore the analyses were repeated with ACPA as additional adjustment factor. Then, no significant results were obtained in any of the cohorts. <h3>Conclusions</h3> This study comprising four cohorts of in total 2766 RA-patients and 8473 X-rays showed that smoking is a risk factor for the progression of joint destruction, but not independent of ACPA-status. <h3>Disclosure of Interest</h3> None Declared
Endoscopic submucosal tunnel dissection of a bronchogenic esophageal cyst
Authors: Xiaowei Tang, Bo Jiang, Wei Gong
Journal: Endoscopy (2014)

A 23-year-old man was admitted to our hospital with the complaint of chest discomfort and dyspnea for the previous 3 months. Upper endoscopy showed a 2.5 × 2.0 cm bulging lesion in the distal esophagus ([Fig. 1]). Endoscopic ultrasound revealed a 1.1 × 2.5 cm hypoechoic cystic lesion arising from the muscularis propria ([Fig. 2]). Endoscopic submucosal tunnel dissection (ESTD) was performed using a hybrid knife (ERBE, Tübingen, Germany), and a cystic mass was observed between the mucosa and the muscular layers of the esophagus. On locating the cyst, its yellowish milky fluid content was aspirated. The cyst wall was excised using endoscopic argon plasma coagulation ([Fig. 3]). Histopathological examination showed a cuboidal epithelium lined cyst wall, which contained cartilage and a few bronchial glands, consistent with a bronchogenic cyst ([Fig. 4]). The patient remained asymptomatic during follow-up.
Alterations in Epithelial Polarity and the Pathogenesis of Disease States
Authors: Franklin H. Epstein, Eileen M. Fish, Bruce A. Molitoris
Journal: New England Journal of Medicine (1994)

Polarized epithelial cells transport ions, water, and macromolecules from one biologic compartment to another. These processes include absorption by enterocytes and renal tubular cells; secretion by hepatocytes, endocrine cells, and exocrine cells; and exchange by alveolar and capillary endothelial cells1,2. The performance of these functions depends on a surface membrane organized into structurally, biochemically, and physiologically distinct apical and basolateral domains containing different ion channels, transport proteins, enzymes, and lipids.The establishment and maintenance of these specialized surface-membrane domains is a multistage process. Alterations at any stage of this process could lead to cell dysfunction and ultimately a . . .
ESD optimisée couplant injection haute pression pulsée et solutions macromoléculaires visqueuses: à propos des 45 premiers cas humains dans 4 centres experts français et belge
Authors: M Pioche, V Lépilliez, P Deprez, M Giovannini, F Caillol, H Piessevaux, J Rivory, O Guillaud, M Ciocirlan, V Hervieu, C Lafon, JC Saurin, T Ponchon
Journal: Endoscopy (2015)

L'ESD a connu deux optimisations majeures depuis les premiers cas avec les solutions visqueuses macromoléculaires qui améliorent le soulèvement et les cathéters bi-fonction couplés à des systèmes d'injection haute pression qui permettent de travailler avec un seul outil. Il n'était jusqu'alors pas possible techniquement de les associer. Le système Nestis Enki II autorise ceci et a montré ses bénéfices par rapport à la méthode classique dans deux précédentes études animales.Nous rapportons les 45 premiers cas d'ESD réalisées sur ce principe à Lyon, Marseille et Louvain dans 4 centres experts.
Abstract CN1-2: Mutations and expression profile to guide treatment in sarcomas and GIST
Authors: Jean-Yves Blay
Journal: Clinical Cancer Research (2010)

Abstract Recent progress in the understanding of the biology of soft tissue sarcomas and locally aggressive connective tissue tumors have enabled the identification of distinct molecular and pathological entities: six molecular subgroups of connective tissue tumors may be distinguished: 1) sarcoma with specific translocations generating fusion gene whose protein products modulate transcription or may act as growth factors (e.g. EWS/Fli1 in Ewing sarcomas, PDGF-col1a1 in DFSP); 2) sarcomas with mutated activated kinases (KIT in GIST); 3) sarcomas with deletion of tumor suppressor genes such as NF1 sarcomas, or rhabdoid tumors (INI1); 4) Sarcomas with simple genetic alterations (mdm2/cdk4 amplification in WD/DD liposarcomas; 5) Sarcomas with gross genetic alterations (e.g. leiomyosarcomas); 6) Tumors with alterations of the intercellular adhesion pathways (aggressive fibromatosis with APC deletion or β catenin mutations). This classification is rapidly evolving. The identification of the “driver” mutation in some of these diseases paved the way for the selection of efficient targeted therapies. One of the most demonstrating examples is the identification of KIT and PDGFRA kinase mutations in GIST which led to the development of imatinib, sunitinib, and more recently hsp90 inhibitors. Imatinib is also active in DFSP, a PDGF driven tumor and in giant cell tumor of the soft part (pigmented villonodular synovitis), an M-CSF driven tumor. Within the 1st molecular subgroup of tumors, in Ewing sarcoma, whose fusion gene product regulates IGFBP3, anti-IGF1R Ab yielded responses in now several phase I and II trials. Within the 4th molecular subgroup of tumors, CDK4 inhibitors and MDM2 inhibitors are currently being investigated in the clinical setting in well differentiated liposarcomas. In addition to these examples, more empiric approaches are also developed, with anti-angiogenics (pazopanib, sorafenib) and mTOR inhibitors (deforolimus) showing efficacy in phase II trials in subtypes of sarcomas; mTOR inhibitors are also currently evaluated in phase II and III trials. The understanding of the driver molecular alterations of these tumors now guides the development of targeted treatment inhibiting driver mutations. Translational research is critical for the development of new treatments, and will be essential to understand the biological mechanisms of response and resistance in these tumor models Citation Information: Clin Cancer Res 2010;16(7 Suppl):CN1-2
Donor Activating <i>KIR2DS1</i> in Leukemia
Authors: Jeffrey M Venstrom, Bo Dupont, Katharine C Hsu, Gianfranco Pittari, Ted A Gooley, Joseph H Chewning, Stephen Spellman, Michael Haagenson, Meighan M Gallagher, Mari Malkki, Effie Petersdorf
Journal: New England Journal of Medicine (2014)

To the Editor: In our original report,1 we used a method based on polymerase-chain-reaction (PCR) amplification developed in our laboratory to perform KIR genotyping.2 We have retyped 1220 of the original 1277 donor samples using three separate published or commercial gene-typing methods (PCR-sequence-specific primers [SSP] and PCR-sequence-specific oligonucleotide probe [SSOP]), and we have repeated the analysis on the retyped cohort. For KIR2DS1, typing was confirmed in 1146 (94%) of the 1220 retested samples and corrected in 74 (6%) of the retested samples. For KIR3DS1, typing was confirmed in 1133 (93%) and corrected in 83 (7%). Differences in typing results came . . .
Trends in consultant clinical activity and the effect of the 2003 contract
Authors: Andrew Will
Journal: Journal of the Royal Society of Medicine (2013)

I read with interest the above article but was confused by the parameters used and the final conclusion that the new contract had failed to realize any increase in consultant clinical activity. This is clearly not the case. Consultants are working harder than ever but in roles that are not captured by measuring their workload as finished consultant episodes (FCE).


The new contract has been good for patients: 


The new contract brought in the concept of supporting programmed activities designed to improve the quality of the work done by consultants.


At a time when reliance on junior doctors has needed to be reduced because of the European Working Time Directive, the contract has been used to redefine the role of consultants from merely directing healthcare to being the primary, hands on, providers of healthcare as well.



Although modern consultants still maintain their traditional role as clinical supervisors, they have increasingly become the main providers of medical treatment in the outpatient clinic and the operating theatre and many have extended working days covering wards. Consultants often see all the patients attending an outpatient session themselves or perform all operating lists personally rather than sharing these duties with a junior as was the case in the past and as a direct result, consultants have less time and can manage fewer patients.


I am surprised that Bloor et al. did not find a greater fall in FCEs because the modern consultant has taken on time-consuming roles that used to be the almost exclusive domain of the doctor in training and this is not something that would be picked up by assessing FCE activity. Thus the Bloor paper significantly underestimates and to some extent misrepresents the clinical workload of the modern consultant.
Radiotherapy in Skin Disease.
Journal: JAMA (1906)

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Perfusion and Blood Pool Scintigraphy for Diagnosing Soft-Tissue Arteriovenous Malformations
Authors: Y Fukuda, Y Murata, I Umehara, T Yamashita, C Ono, T Iwai, H Shibuya
Journal: Clinical Nuclear Medicine (1999)

Six arteriovenous malformations were assessed to determine the effectiveness of perfusion and blood pool scintigraphy to diagnose arteriovenous malformations of soft tissue.After injection of Tc-99m RBC or Tc-99m DTPA-HSA, dynamic perfusion and early and delayed blood pool images were analyzed.Four of six arteriovenous malformations showed increased activity on perfusion images and slightly increased activity on blood pool images; the remaining two arteriovenous malformations showed increased activity on perfusion and normal activity on blood pool studies.This expansion of the authors' previous studies of hemangiomas shows that perfusion and blood pool scintigraphy are useful methods to differentiate arteriovenous malformations from various types of hemangiomas.
Iodine-131 Uptake in Focal Bronchiectasis Mimicking Metastatic Thyroid Cancer
Authors: HO-CHUN SONG, YOUNG-JUN HEO, SEONG-MIN KIM, HEE-SEUNG BOM
Journal: Clinical Nuclear Medicine (2003)

SONG, HO-CHUN M.D.; HEO, YOUNG-JUN M.D.; KIM, SEONG-MIN M.D.; BOM, HEE-SEUNG M.D., PH.D. Author Information
Commentary: Lymphohematogenous Spread of Asbestos
Authors: Arnold Brown
Journal: Environmental Health Perspectives (1974)

I would like to make a few comments and pose a question or two concerning the question of the lymphohematogenous spread of asbestos. The paper by Godwin and Jagatic (1) is one of the more important publications that I have come across concerning the distribution of fibers in patients in whom there was both asbestosis and mesothelioma. This study was done very carefully and demonstrated rather nicely the presence of fibers in various organs throughout the body including the spleen and lymph nodes, hilar lymph nodes particularly. Another study with of considerable interest is by Kanazawa et al. (2). They injected crocidolite subcutaneously in rats and found the regional lymph nodes to be rather heavily involved by these fibers. The fact that these fibers apparently can cross various natural barriers such as the endothelial wall and the gastric, small intestinal, and even colonic epithelium seems to be fairly well shown. This raises several very interesting questions. Those of us who have had an opportunity over the years to look at the gastric and intestinal mucosa are very impressed by the dynamic nature of this epithelial surface. The epithelial surface of the gastro intestinal tract is a highly dynamic structure, the cells changing shape and size continuously. The renewal rate varies somewhat, but is in the range of 2-5 days. So when you have a very dynamic situation all sorts of things can happen, including the insorption of relatively large particles, which you would not ordinarily predict from the static,
AB0848 Rituximab treatment for spondyloarthritis. A nationwide series: Data from the air registry
Authors: D. Wendling, M. Dougados, F. Berenbaum, O. Brocq, T. Schaeverbeke, B. Mazieres, C. Marcelli, J.-M. Le Parc, P. Bertin, M. Robin, J. Sibilia, P. Lafforgue, C. Prati, B. Combe, J.-E. Gottenberg
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Only few data are available about rituximab (RTX) in spondyloarthritis. <h3>Objectives</h3> The aim of this study was to evaluate efficacy and safety of rituximab treatment in several subsets of spondyloarthritis (SpA) using the data of the AIR (AutoImmunity and Rituximab) registry. <h3>Methods</h3> All patients receiving rituximab (RTX) for spondyloarthritis, and included in the AIR registry from September 2005 to September 2010, were eligible for the study, and retrospectively analysed. Patient characteristics, indications, therapy regimen, and tolerance and efficacy of RTX were collected at baseline and at 3- and 6-month follow-up, then every 6 months or at disease relapse. The response to treatment was evaluated by BASDAI reduction over 2 units (on a 0-10 scale) for axial disease, joint count reduction over 20% for peripheral disease, and CRP reduction. Side effects were recorded. <h3>Results</h3> Among the 595 patients included in the AIR registry, 26 SpA patients, from 13 centres were reported; mean age 51 years, 13 men, ankylosing spondylitis (10), undiffenciated spondyloarthritis (7), and psoriatic arthritis (9). The mean disease duration was 8.8 years (1-40), extra articular features: psoriasis 12 cases, uveitis 4 cases, Crohn's disease 3 cases. The mean number of DMARDs before rituximab was 2.4, a previous TNF blocker has been used in 23 cases; rituximab treatment courses was a mean of 1.5 (1 to 5), with a mean follow up of 17.8 months, and a total of 35.6 patients-years. Efficacy was evaluable in 23 cases, with a response between 3 to 7 months after treatment in 11 cases: 3 out of 3 anti-TNF naïve patients and 8 out of 20 anti-TNF non responder patients. No differences were seen between responders and non responders for baseline CRP, HLA-B27 presence, gender, disease duration, extra articular features, immunoglobulin serum levels, clinical presentation (axial/peripheric) or initial diagnosis (AS, PsA, SpA). Safety: one severe infection, one cardiac failure, 2 cases of psoriasis deterioration, 2 uveitis episodes (one de novo) were recorded. <h3>Conclusions</h3> In this nationwide open experience of rituximab on several subsets of spondyloarthritis, we saw only a moderate efficacy, more evident for patients naive for anti TNF agents. <h3>Disclosure of Interest</h3> None Declared