tbuckley/cabot-search huggingface dataset:
Cardiovascular events and death in Japanese patients with chronic kidney disease
Authors: Kenichi Tanaka, Tsuyoshi Watanabe, Ayano Takeuchi, Yasuo Ohashi, Kosaku Nitta, Tadao Akizawa, Seiichi Matsuo, Enyu Imai, Hirofumi Makino, Akira Hishida
Journal: Kidney International (2016)

The incidence of cardiovascular disease (CVD) is higher in patients with chronic kidney disease (CKD) than in the general population, and the risk of CVD increases with reductions in renal function. However, the incidence of CVD in Japanese patients with CKD has not been sufficiently investigated. To measure this we conducted the Chronic Kidney Disease Japan Cohort (CKD-JAC) Study over four years in 2,966 Japanese patients with CKD to examine the incidence of CVD and all-cause death. These patients had an estimated glomerular filtration rate (eGFR) of 10–59 ml/min/1.73 m<sup>2</sup>, were under nephrologist care, and pooled from 17 medical institutions in Japan. At the median follow-up of 3.9 years, 69 patients had died, 217 had cardiovascular events, and 514 started maintenance dialysis therapy. The incidences of cardiovascular events were 11.9, 19.1, 25.0, and 39.4 per 1,000 person-years at eGFRs of 45–59, 30–44, 15–29, and under 15 ml/min/1.73 m<sup>2</sup>, respectively. The adjusted Cox proportional hazards models showed that the risk of cardiovascular events increased as the eGFR decreased, with a significant difference only between CKD stage G5 (eGFR: under 15 ml/min/1.73 m<sup>2</sup>) and CKD stage G3a (eGFR: 45–59 ml/min/1.73 m<sup>2</sup>) (hazard ratio 3.16, 95% confidence interval 1.28 to 7.76). Thus, the risk of CVD and all-cause death was related to the decrease in eGFR, but not necessarily elevated in proportion to progression of the CKD stage in Japanese patients with predialysis CKD under a nephrologist's care.
FRI0373 The Clinical and Demographic Features of Relapsing Polychondritis: A Nationwide Study: Table 1.
Authors: H. Emmungil, A. Erden, O. Küçükşahin, O. Zengin, S. Ermurat, K. Gök, A. Doğru, M. Kalfa, L. Akyol, F. Erbasan, M. Çınar, M.A. Balcı, A. Yazıcı, S. Yavuz, B. Göker, A. Sarı, M. Turgay, A.M. Onat, B. Kısacık, Y. Pehlivan, S. Şenel, M. Şahin, M. Sayarlıoğlu, Ö.N. Pamuk, A. Çefle, S.Z. Aydın, U. Kalyoncu
Journal: Annals of the Rheumatic Diseases (2016)

<h3>Background</h3> Relapsing polychondritis (RP) is a rare systemic and inflammatory disease. <h3>Objectives</h3> to assess clinical features, management and prognosis in RP. <h3>Methods</h3> Retrospective medical records were collected from 16 centers for 37 patients with RP diagnosed by Michet criteria. Data included patients9 demographics, clinical features, laboratory findings and outcome. <h3>Results</h3> A total of 37 patients, (Male/female=19/18) with a mean disease onset of 45.7±11.8 years and median follow up period is 20 (1–360) months were enrolled. The most common initial complaints and organs involved were showed in table 1. Mean lead time to diagnose was 28.6±54.3 (0–228) months. Four patients had a known history of cartilage injury before the RP diagnosis (Three goiter operation and 1 resuscitation due to a drowning). Twelve of the patients (32.4%) had also various autoimmune or hematologic diseases. After the diagnosis, moderate or high dose prednisone (n=37, 100%), plus methotrexate (n=15, 40.5%) or azathioprine (AZA) (n=11, 29.7%) or hydroxychloroquine (HQ) (n=3, 8.1%) or cyclophosphamide (CYP) (n=2, 5.4%), or (AZA+ HQ n=3, 8.1%) treatments were initiated. In the case of resistant disease, CYP (n=6, %16.2), tocilizumab (n=2, 5.4%), etanercept (n=1, 2.7%), infliximab (n=1, 2.7%) and bevacizumab (n=1, 2.7%) treatments were given. Due to tracheal stenosis surgery applied to 2 patients, one patient died due to respiratory collapse, 21 patients on remission without any complications, 13 (35.1%) patients had developed tracheal stenosis (n=5, 13.5%), major airway cartilage loss (n=5, 13.5%), auricular collapse (n=2, 5.4%), nasal collapse (n=3, 8.1%), subglottic stenosis (n=2, 5.4%), hearing loss (n=5, 13.5%), vision loss (n=1, 2.7%) and deforming arthritis (n=1, 2.7%). In the univariate analysis, only major airway involvement had a relationship with complication development. (OR 12, 95% CI 1.97–72.8, p=0.007) <h3>Conclusions</h3> RP is a rare disease which diagnosis is commonly delayed and lead to cartilage loss. RP developed after trauma in 4 patients, possibly trauma can be blamed as an etiologic factor. Awareness and early diagnosis results with better prognosis <h3>Disclosure of Interest</h3> None declared
Diffuse Large B-Cell Transformation in Nodular Lymphocyte Predominant Hodgkin Lymphoma: Incidence, Risk Factors and Outcomes After a Forty-Year Experience From a Single Institution
Authors: Saad J. Sirop, Thomas M Habermann, William R Macon, Kay M. Ristow, Stephen M Ansell, Joseph P Colgan, Patrick B. Johnston, David J. Inwards, Svetomir N. Markovic, Ivana N. Micallef, Carrie Thompson, Luis F. Porrata, James A. Martenson, James R Cerhan, Thomas E. Witzig, Grzegorz S. Nowakowski
Journal: Blood (2012)
Spectrum of Phenotypic Manifestations of a Novel c1339A&gt;C, pS447R Germline GATA2 Mutation
Authors: Samith T. Kochuparambil, Amie E Jackson, Mark R. Litzow, Shakila Khan, Vilmarie Rodriguez, William J. Hogan, Roshini Abraham, Mrinal M. Patnaik
Journal: Blood (2014)
Interaction domains of the tumor suppressor Pdcd4 and translation initiation factors eIF4A and eIF4G
Authors: Halina I. Zakowicz, Hsin-Sheng Yang, Alexander Wlodawer, Nicole Laronde-Leblanc, Nancy H. Colburn
Journal: Cancer Research (2004)

Proc Amer Assoc Cancer Res, Volume 46, 2005

4619 

Pdcd4 (programmed cell death 4) is a novel transformation suppressor protein highly expressed in JB6 mouse epidermal P- (transformation resistant) cells but not P+ (transformation sensitive) cells. The P- cells, unlike the P+ cells, do not undergo transformation to tumor cells in response to tumor promoters such as TPA and EGF. Expression of Pdcd4 in P+ cells renders them resistant to transformation, thus establishing Pdcd4 as a transformation suppressor. The eukaryotic translation initiation factor 4A (eIF4A) is a 407 amino acid protein that associates with Pdcd4. eIF4A contains ten highly conserved domains and is part of a family of DEAD-box RNA helicases with ATP hydrolysis activity. In binding eIF4G at both its middle region (eIF4GM) and C-terminus (eIF4GC), eIF4A is thought to utilize energy from ATP to unwind secondary/tertiary RNA structure. This allows recruitment of the 40S ribosomal unit to the 5’ end of the mRNA and subsequent translation initiation. Pdcd4 is thought to inhibit eIF4A by binding to it and to eIF4GM, while competing with eIF4GC for binding to eIF4A. We hypothesize that by binding eIF4A at its ten highly conserved domains, Pdcd4 may inhibit this protein’s ATP hydrolysis, helicase and/or eIF4G binding activities, and this is the mechanism by which Pdcd4 inhibits neoplastic transformation. To map the interaction domains of eIF4A with Pdcd4 and eIF4G, point mutants of eIF4A were made at its ten highly conserved domains. Using mammalian two-hybrid assays, pull-downs, and immunoprecipitations, five eIF4A mutants completely lost binding to Pdcd4 while four eIF4A mutants retained wild type levels of binding. The residues that, when mutated, inactivated Pdcd4 binding were residues that specified ATP binding, ATP hydrolysis, or RNA binding. With the exception of Q motif mutant eIF4AP56L, the eIF4A mutants inactivated for Pdcd4 binding were inactivated for binding to eIF4G (GM, GC, or both) and for enhancing translation. Several eIF4A mutants showing wild type level binding to Pdcd4 were also inactivated for binding to eIF4G and for enhancing translation. Thus, significant dissociation of eIF4A’s Pdcd4 and eIF4G binding regions appears to occur. Because three of the four eIF4A mutants that retained Pdcd4 binding also suppressed translation activity in a dominant-negative manner, the structure that defines the Pdcd4-binding domain of eIF4A may be necessary but is insufficient for translation. A ribbon and space-fill model of eIF4A shows regions important for binding to Pdcd4 and/or eIF4G lying on the perimeters of the hinge area of eIF4A. A competition experiment revealed that Pdcd4 competes with eIF4GC for binding to eIF4A. In summary, the Pdcd4-binding domains on eIF4A impact both binding to eIF4G and translation initiation in cells.
Prognosis and risk factors of insulin resistance and abnormal glucose metabolism in patients with polycystic ovary syndrome: a single-centre, retrospective, database study
Authors: Na Di, Yaxiao Chen, Xiaoli Chen, Lin Li, Xiaomiao Zhao, Ping Pan, Linlin Jiang, Manlin Liu, Jia Huang, Hui Li, Hui Huang, Dongzi Yang
Journal: The Lancet Diabetes & Endocrinology (2016)
P0266 : Adeno-Associated Virus 2 (AAV2) induces recurrent insertional mutagenesis in Human Hepatocellular Carcinomas
Authors: J.C. Nault, S. Datta, A. Franconi, S. Imbeaud, M. Mallet, G. Couchy, E. Letouzé, C. Pilati, B. Verret, J.F. Blanc, C. Balabaud, J. Calderaro, A. Laurent, M. Lextexier, P. Bioulac-Sage, F. Calvo, J. Zucman-Rossi
Journal: Journal of Hepatology (2015)
Response by Grimaldi et al to Letter Regarding Article, “Tropical Endomyocardial Fibrosis: Natural History, Challenges, and Perspectives”
Authors: Antonio Grimaldi, Ana-Olga Mocumbi, Kumar Narayanan, Eloi Marijon
Journal: Circulation (2016)

][4] We agree that a significant body of evidence points to a role for eosinophils, and accordingly we have presented this as 1 of the potential hypotheses for the genesis of EMF in our article.However, as we point out, issues of geographical mismatch with parasitic infestations, lack of universal presence of eosinophils, and associations with certain dietary patterns do not allow at present for a clear picture of causality to emerge.Improvements in socioeconomic conditions, while allowing for a decline of parasitic infections, may also result in changes in dietary habits that can hypothetically lead to a decline in EMF related to ingestion of toxins or microelement deficiency.It may well be possible that fibrosis and cavity obliteration represent a common endpoint to multiple pathways triggered by various factors or an interplay of them.We certainly agree with Kothari on the need for further enthusiastic and rigorous research into the role of eosinophils, but until such time that all the facets in the pathogenesis of this still mysterious disease are completely decoded, we must remain open to other potential etiologies of EMF.
Life-threatening NLRC4-associated hyperinflammation successfully treated with IL-18 inhibition
Authors: Scott W. Canna, Charlotte Girard, Louise Malle, Adriana de Jesus, Neil Romberg, Judith Kelsen, Lea F. Surrey, Pierre Russo, Andrew Sleight, Eduardo Schiffrin, Cem Gabay, Raphaela Goldbach-Mansky, Edward M. Behrens
Journal: Journal of Allergy and Clinical Immunology (2016)
Qki deficiency maintains stemness of glioma stem cells in suboptimal environment by downregulating endolysosomal degradation
Authors: Takashi Shingu, Allen L Ho, Liang Yuan, Xin Zhou, Congxin Dai, Siyuan Zheng, Qianghu Wang, Yi Zhong, Qing Chang, James W Horner, Brandon D Liebelt, Yu Yao, Baoli Hu, Yiwen Chen, Gregory N Fuller, Roeland G W Verhaak, Amy B Heimberger, Jian Hu
Journal: Nature Genetics (2016)
Different Number of AML1/ETO Transcripts in Single Leukemic Cell, Estimated by Combined Measurement of MRD by FISH and Real-Time PCR, Is a Powerful Predictor of Relapse.
Authors: Hideaki Maeba, Ryosei Nishimura, Rie Kuroda, Toru Horisawa, Yutaka Saikawa, Shoichi Koizumi
Journal: Blood (2007)
P2.39: Long-Term OS for Patients With Advanced NSCLC Enrolled in the KEYNOTE-001 Study of Pembrolizumab
Authors: Suresh Ramalingam, Rina Hui, Leena Gandhi, Enric Carcereny, Enriqueta Felip, Myung-Ju Ahn, Joseph P. Eder, Ani S. Balmanoukian, Natasha Leighl, Charu Aggarwal, Leora Horn, Amita Patnaik, Gary W. Middleton, Matthew Gubens, Matthew Hellmann, Jean-Charles Soria, Gregory M. Lubiniecki, Jin Zhang, Bilal Piperdi, Edward B. Garon
Journal: Journal of Thoracic Oncology (2016)
Rituximab Maintenance Therapy Is an Effective Therapy in over-Sixties with Mantle Cell Lymphoma
Authors: Norihito Inoue, Noriko Nishimura, Anna Takahashi, Yoshiharu Kusano, Tadahiro Gunji, Hideaki Nitta, Kyoko Ueda, Yuko Mishima, Masahiro Yokoyama, Yasuhito Terui, Kiyohiko Hatake
Journal: Blood (2015)
AB0651 Usefulness of Neutrophil To Lymphocyte Ratio in Prediction of Lung Involvement in Patient with Systemic Sclerosis
Authors: W.S. Lee, Y.-M. Lee, M.-J. Hong, C.-H. Lee, M.S. Lee, S.-I. Lee, W.-H. Yoo
Journal: Annals of the Rheumatic Diseases (2016)

<h3>Background</h3> Both neutrophil-to-lymphocyte ratio (NLR) and platelet-to-lymphocyte (PLR) are reported to be increased in various inflammatory diseases, but there clinical significance in systemic sclerosis (SSc) remains unclear <h3>Objectives</h3> The aim of the study is to evaluate usefulness of neutrophil to lymphocyte ratio in diagnosis of systemic sclerosis and in prediction of lung involvement such as pulmonary fibrosis. <h3>Methods</h3> The medical records of 88 SSc patients and 50 healthy controls were retrospectively reviewed. NLR, PLR between SSc patients and healthy controls were compared, and correlation between these indexes and lung involvement were analyzed. Exclusion criteria included active infection and/or the presence of any hematological, cardiovascular or metabolic disorder. <h3>Results</h3> The NLR and PLR were found to be significantly higher in SSc patients when compared to the healthy control (NLR: 3.95±6.59 vs 2.00±1.07, p&lt;0.01, PLR: 163.87±101.12 vs 126.33 ±42.31, p&lt;0.05). SSc patients with lung involvement had higher NLR and PLR levels than those without lung involvement (p&lt;0.01, p&lt;0.05). NLR was negatively correlated with forced vital capacity (FVC)(r=-0.341, p&lt;0.01) but not diffusing capacity for carbon monoxide (DLCO). Receiver-operating characteristics analysis (ROC) of NLR to predict lung involvement in SSc showed that the area under the curve (AUC) was 0.763. The cut-off NLR value for prediction of lung involvement was determined as 2.59. (sensitivity, 0.700;specificity, 0.729; p&lt;0.01) <h3>Conclusions</h3> NLR may be a promising marker that reflects lung involvement in patients with SSc and values greater than 2.59 were useful in prediction of lung involvement. <h3>Disclosure of Interest</h3> None declared
Characterization of Bcr-Abl Positive Leukemic Cells under Long-Term In Vitro Treatment with Telomerase Inhibitor BIBR1532.
Authors: Ute Brassat, Stefan Balabanov, Ulrike Hartmann, Daniel Rössler, Kerstin Borgmann, Judith Dierlamm, Tim H. Brummendorf
Journal: Blood (2006)
Adherence to Oral Tyrosine Kinase Inhibitor Therapy: Results of a Self-Reported Patient Survey
Authors: Stuart L. Goldberg, Miriam S Aioub, William H Beluch, Lacey Sara Kaplan, Tarundeep Singh, Jayshree Shah, Genique Stanislaus, Sora Limor, Alyona Weinstein, Elizabeth Jones, Kenneth Granholm, Katarzyna Szyperek, Melanie Marcincak, Michele Hanrahan, Jamie L Yaniga, Jennifer Lynn Llanes, Sandra Palomino, Lissette Pajaro, Lynne Larsen, Peggy Stone, Anita Vargas, Rebecca Hirsch, Diane Powell
Journal: Blood (2011)
Extended TNF Genotyping Identifies TNF -857T as a Risk Factor for Acute Graft-Versus-Host Disease Following Allogeneic Hematopoietic Stem Cell Transplantation.
Authors: Charles Mullighan, Sue L. Heatley, Natalie R. Villalta, Kathleen V. Doherty, Silke Danner, Uwe Hahn, Kenneth Bradstock, Anthony P. Schwarer, Jeffrey Szer, Peter G. Bardy
Journal: Blood (2006)
Prognostic Analysis of Hodgkin Lymphoma (HL) in JAPAN
Authors: Rumiko Okamoto, K. Itoh, T. Kinoshita, T. Watanabe, K. Yoshimura, T. Chou, M. Ogura, M. Hirano, H. Asaoku, M. Kurosawa, Y. Maeda, K. Omachi, Y. Moriuchi, M. Kasai, K. Ohnishi, N. Takayama, Y. Morishima, K. Tobinai, H. Kaba, S. Yamamoto, H. Fukuda, M. Kikuchi, T. Yoshino, Y. Matsuno, T. Hotta, M. Shimoyama
Journal: Blood (2008)
A Phase I Study of Milatuzumab, a Humanized Anti-CD74 Antibody, and Veltuzumab, a Humanized Anti-CD20 Antibody, In Patients with Relapsed and Refractory B-Cell Non-Hodgkin's Lymphoma.
Authors: Beth Christian, Lapo Alinari, Christian Tyler Earl, Emily Wilding, Carl Quinion, Mark Lustberg, Don M Benson, Jeffrey A. Jones, John C. Byrd, William A. Wegener, David M. Goldenberg, Robert A. Baiocchi, Kristie A. Blum
Journal: Blood (2010)
Covering Undocumented Immigrants — State Innovation in California
Authors: Rachel Fabi, Brendan Saloner
Journal: New England Journal of Medicine (2016)

Interview with Rachel Fabi on recent legislative measures to extend insurance coverage for undocumented immigrants in California. (06:08)Download Insuring undocumented U.S. immigrants would be a key step toward achieving universal health care coverage. In a hostile national political climate, recent legislative moves in the California legislature provide test cases for laws that could be replicated in other states.
OC-041 A Novel, Integrated Care Pathway for Irritable Bowel Syndrome (IBS) Using Faecal Calprotectin (FC) to Facilitate Direct Access to a Specialist Dietetic-Led Refractory IBS Service
Authors: C Oldale, A Di Mambro, L Materacki, S Waterman
Journal: Gut (2016)

<h3>Introduction</h3> IBS is a common, chronic condition, incurring significant financial and time costs in both primary care and gastroenterology services. Symptoms may persist despite initial dietary, lifestyle and pharmacological interventions prompting referral for specialist gastroenterology input and investigation. Use of FC can exclude differential diagnoses such as inflammatory bowel disease without luminal investigation. Up to 75% of patients with IBS report symptomatic benefits with strict adherence to a low FODMAP diet,<sup>1</sup> but this requires expert dietetic support. A pathway was indicated to facilitate direct access from primary care to specialist dietetic services for patients who do not require gastroenterologist review. <h3>Methods</h3> Patients aged 16–45 with IBS symptoms according to Rome Criteria are eligible for this care pathway (Figure 1). In patients with persisting symptoms despite interventions as per NICE-guidance,<sup>2</sup> FC informs further management. Patients with FC &lt; 150 µg/g faeces can be referred to the dietetic-led refractory IBS service. This includes comprehensive symptom assessment, supported implementation of dietary exclusions with a low FODMAP diet followed by dietary re-challenge to identify triggers and optimise long-term IBS management. Patients with no symptomatic improvement following dietary manipulation are directly referred for gastroenterology review. Patients with an intermediate FC (51–149 µg/g faeces) undergo repeat FC after 3 months. Escalation of FC level prompts further investigation and consultant review. A consultant and specialist dietitian led education program was provided to regional GPs on practical implementation of the pathway. <h3>Results</h3> The pathway and IBS service will be audited prospectively based on clinical outcomes, FC use in primary care and impact on referral to gastroenterology and endoscopy services. <h3>Conclusion</h3> A comprehensive IBS care pathway and direct access service is now in place in Gloucestershire. Improvements to quality of care for IBS patients through provision of timely, appropriate and successful treatment options and prevention of unnecessary referral to gastroenterology and endoscopy services will be monitored. <h3>References</h3> 1 Halmos, <i>et al</i>. A diet low in FODMAPs reduces symptoms of irritable bowel syndrome. <i>Gastroenterology</i> 2014;<b>146</b>:67–75 2 NICE. <i>Irritable bowel syndrome in adults: Diagnosis and management of irritable bowel syndrome in primary care. NICE Guidance CG61</i> February 2008. Guideline addendum 2015. <h3>Disclosure of Interest</h3> None Declared
PTH-093 Portal Vein Thrombosis
Authors: A Malik, A Yeoman, M Allison, M Czajkowski
Journal: Gut (2016)

<h3>Introduction</h3> Portal vein thrombosis (PVT) is defined as the presence of thrombus in the trunk of PV and/or its right and left intra-hepatic branches. PVT can be classified as acute or chronic, intra or extra-hepatic and occlusive or non-occlusive. Patients may be asymptomatic or present with upper GI bleeding or abdominal pain. PVT in cirrhotic patients can present with acute decompensation such as ascites or variceal bleeding. <h3>Methods</h3> A retrospective review of all radiological diagnoses of PVT was done with a view to understanding the aetiology, clinical spectrum, treatment and prognosis of patients managed under a large district hospital. <h3>Results</h3> A total of 115 patients, median age 62 years (range 25 to 90) were diagnosed with PVT between 2010 and 2015, of whom 71 (62%) were male. Usual indications for radiological investigations were abdominal pain, weight loss and decompensation or routine surveillance in cirrhotic patients. PVT was intra-hepatic alone in 29 patients and extra-hepatic with or without intra-hepatic extension in the rest. Cavernous transformation was reported in 11 patients. PVT was most commonly seen in association with abdominal malignancy (55 cases – 48%) being due to HCC in 21 cases and other local or metastatic abdominal malignancy in 34. PVT was observed to be due to pancreatitis in 21 cases, liver cirrhosis without HCC in 15, acute diverticulitis/cholecystitis in 6, post surgical in 4 with no clear cause identified in just 14 cases (12%). Thrombophilia screening was performed in 11/14 patients with unclear aetiology and was positive in 3 (1 JAK-2 positive, 1 elevated anti-b2GP1 antibodies, 1 low in both protein C and S, rest negative), 2/15 patients with liver cirrhosis (both negative) and 4/86 (1 positive for lupus anti-coagulant) of remaining patients. In total 24 patients were anticoagulated whilst 3 patients were already on warfarin for atrial fibrillation. Of these, 10 were patients of unclear aetiology, 4 with cirrhosis without HCC, 3 had diverticulitis, 3 local or metastatic malignancy, 2 pancreatitis, 1 cholecystitis and 1 post surgical. Eleven of the 15 patients with cirrhosis and PVT died, typically from hepatic decompensation with a median life expectancy of 8 months (range 1–48 months). Patients who were anticoagulated survived for 12 months as opposed to 4 months for those not anticoagulated. <h3>Conclusion</h3> PVT has a wide aetiological spectrum and management strategies are highly variable reflecting the diversity of causes. Anticoagulation was most likely to be commenced in those with no clear cause even in the absence of thrombophilia. This study confirms that PVT in the context of cirrhosis is an adverse prognostic indicator even in the absence of HCC. <h3>Disclosure of Interest</h3> None Declared
Phase 1 Dose-Escalation Study of MLN4924, a Novel NAE Inhibitor, in Patients with Multiple Myeloma and Non-Hodgkin Lymphoma.
Authors: Jatin J Shah, Andrzej J Jakubowiak, Owen A O’Connor, Robert Z Orlowski, Molly Patterson, Donald Harvey, Allison J Berger, Alice McDonald, George Mulligan, Lilli Petruzzelli, Michael D Pickard, Peter G Smith, Karthik Venkatakrishnan, Sagar Lonial
Journal: Blood (2009)
Thrombophilia and Cardiovascular Risk Factors On the Absolute Risk of First and Recurrent Venous Thrombosis. Results From a Retrospective Family Cohort Study Involving 2097 Relatives.
Authors: Anja B.U. MÄkelburg, Saskia Middeldorp, Karly Hamulyàk, Martin Prins, Harry R Büller, Willem M. Lijfering
Journal: Blood (2009)