tbuckley/cabot-search huggingface dataset:
Relationship of c-myc Amplification to Progression of Breast Cancer From In Situ to Invasive Tumor and Lymph Node Metastasis
Authors: P. H. Watson, J. R. Safneck, K. Le, D. Dubik, R. P. C. Shiu
Journal: JNCI Journal of the National Cancer Institute (1993)

Journal Article Relationship of c-myc Amplification to Progression of Breast Cancer From In Situ to Invasive Tumor and Lymph Node Metastasis Get access Peter H. Watson, Peter H. Watson Department of Physiology, Faculty of Medicine, University of ManitobaCanada Correspondence to : Peter H. Watson, M.B., Department of Physiology, Faculty of Medicine, University of Manitoba, 770 Bannatyne Ave., Winnipeg, MB, R3E OW3, Canada. Search for other works by this author on: Oxford Academic PubMed Google Scholar Janice R. Safneck, Janice R. Safneck Department of Pathology, Faculty of Medicine, University of ManitobaCanada Search for other works by this author on: Oxford Academic PubMed Google Scholar Khuong Le, Khuong Le Department of Physiology, Faculty of Medicine, University of ManitobaCanada Search for other works by this author on: Oxford Academic PubMed Google Scholar Don Dubik, Don Dubik Department of Physiology, Faculty of Medicine, University of ManitobaCanada Search for other works by this author on: Oxford Academic PubMed Google Scholar Robert P. C. Shiu Robert P. C. Shiu Department of Physiology, Faculty of Medicine, University of ManitobaCanada Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 85, Issue 11, 2 June 1993, Pages 902–907, https://doi.org/10.1093/jnci/85.11.902 Published: 02 June 1993 Article history Received: 08 December 1992 Accepted: 03 March 1993 Published: 02 June 1993
Resource Allocation in Neonatal and Medical ICUs
Authors: JOHN D. LANTOS, MANI MOKALLA, WILLIAM MEADOW
Journal: American Journal of Respiratory and Critical Care Medicine (1997)

This study compared resource allocation to patients who eventually die in neonatal ICUs (NICUs) and adult medical ICUs (MICUs). It was performed via retrospective, chart review study at ICUs at the University of Chicago—an inner city, tertiary care, academic medical center. All patients were admitted to the neonatal, general medical, or coronary ICU during 1 calendar yr. Overall mortality in the NICU (66/827; 7.9%) was significantly lower than in the adult ICUs (219/1320; 16.5%) (p < 0.001). However, mortality for the smallest newborns ( < 751 g; 51% mortality) was higher than for the oldest adults ( > 84 yr; 30% mortality) (p = 0.05). Fifty-six percent (37/66) of all neonates who died in the NICU did so within the first 48 hr of life. In contrast, nearly two-thirds (134/219) of adult ICU deaths occurred after 48 hours in the ICU (p < 0.02). The percentage of ICU bed-days devoted to nonsurviving adults (28.8%) was significantly larger than the percentage of NICU bed-days devoted to nonsurviving babies (7.8%). Even among babies at greatest risk to die (birth weight < 751 g), the percentage of NICU bed-days allocated to nonsurviving infants was less than 20%. In contrast, for the oldest ICU patients ( > 84 yr) this value exceeded 50%, for ICU patients > 84 yr old who required mechanical ventilation, the percentage of ICU bed-days allocated to nonsurvivors approached 90%. Care for the elderly in MICUs involves a far greater proportional expenditure of money toward those who will not survive than does care for newborns in NICUs. To the extent that allocation decisions are driven by concerns about distributive justice and the efficient use of scarce resources, it would be more justifiable to ration intensive care for the very old than the very young.
Decreased frequency of HLA-DR13DR6 in Wegener's granulomatosis
Authors: E. Christiaan Hagen, Coen A. Stegeman, Joe D'Amaro, Geziena M.T. Schreuder, Simon P.M. Lems, Jan Willem Cohen Tervaert, Gijs MTh de Jong, Ronald J. Hené, Cees G.M. Kallenberg, Mohammed R. Daha, Fokko J. van der Woude
Journal: Kidney International (1995)
Faecal carcinoembryonic antigen in colorectal cancer patients.
Authors: R S Stubbs, D M Nadkarni, H A Monsey
Journal: Gut (1986)

Carcinoembryonic antigen (CEA) has been measured in the faeces of large bowel cancer patients and control subjects to determine whether this measurement might be a useful aid in the diagnosis of large bowel cancer. The mean faecal CEA in 24 cancer patients fell significantly from 10.43 +/- 2.39 micrograms/g pre-operatively to 3.61 +/- 0.72 micrograms/g postoperatively (p less than 0.05). Pre-operative values were not related to either tumour stage or serum CEA. In 20 patients with no known colorectal disease the mean faecal CEA was 5.43 +/- 1.95 micrograms/g which was significantly lower than the mean pre-operative value in the cancer patients (p less than 0.05). In 14 patients with a variety of benign colonic diseases the mean faecal CEA was 7.12 +/- 1.39 micrograms/g which was not significantly different from the mean pre-operative value in the cancer patients. Considerable overlap of values was observed between individual cancer and control patients making the test, as presently carried out, non-discriminatory. If the potential for making the test more cancer specific can be realised, however, faecal CEA determination may permit discrimination between cancer and non-cancer patients at a relatively early stage of disease.
Eligibility for concurrent chemotherapy and radiotherapy of locally advanced lung cancer patients: a prospective, population-based study
Authors: D. De Ruysscher, A. Botterweck, M. Dirx, M. Pijls-Johannesma, R. Wanders, M. Hochstenbag, A.-M. C. Dingemans, G. Bootsma, W. Geraedts, J. Simons, C. Pitz, P. Lambin
Journal: Annals of Oncology (2008)
Impairment of glucose-induced insulin secretion in human pancreatic islets transplanted to diabetic nude mice.
Authors: L Jansson, D L Eizirik, D G Pipeleers, L A Borg, C Hellerström, A Andersson
Journal: Journal of Clinical Investigation (1995)

Hyperglycemia-induced beta-cell dysfunction may be an important component in the pathogenesis of non-insulin-dependent diabetes mellitus. However, most available data in this field were obtained from rodent islets. To investigate the relevance of this hypothesis for human beta-cells in vivo, human pancreatic islets were transplanted under the renal capsule of nude mice. Experimental groups were chosen so that grafted islets were exposed to either hyper- or normoglycemia or combinations of these for 4 or 6 wk. Grafts of normoglycemic recipients responded with an increased insulin release to a glucose stimulus during perfusion, whereas grafts of hyperglycemic recipients failed to respond to glucose. The insulin content of the grafts in the latter groups was only 10% of those observed in controls. Recipients initially hyperglycemic (4 wk), followed by 2 wk of normoglycemia regained a normal graft insulin content, but a decreased insulin response to glucose remained. No ultrastructural signs of beta-cell damage were observed, with the exception of increased glycogen deposits in animals hyperglycemic at the time of killing. It is concluded that prolonged exposure to a diabetic environment induces a long-term secretory defect in human beta-cells, which is not dependent on the size of the islet insulin stores.
A Likelihood Method for Detecting Trait-Dependent Shifts in the Rate of Molecular Evolution
Authors: Itay Mayrose, Sarah P. Otto
Journal: Molecular Biology and Evolution (2010)

Rate heterogeneity within groups of organisms is known to exist even when closely related taxa are examined. A wide variety of phylogenetic and dating methods have been developed that aim either to test for the existence of rate variation or to correct for its bias. However, none of the existing methods track the evolution of features that account for observed rate heterogeneity. Here, we present a likelihood model that assumes that rate variation is caused, in part, by species’ intrinsic characteristics, such as a particular life-history trait, morphological feature, or habitat association. The model combines models of sequence and character state evolution such that rates of sequence change depend on the character state of a lineage at each point in time. We test, using simulations, the power and accuracy of the model to determine whether rates of molecular evolution depend on a particular character state and demonstrate its utility using an empirical example with halophilic and freshwater daphniids.
Progress in the surveillance of respiratory syncytial virus (RSV) in Europe: 2001-2008
Authors: T J Meerhoff, A Mosnier, F Schellevis, W  J Paget, None the EISS RSV Task Group
Journal: Eurosurveillance (2009)

Respiratory syncytial virus (RSV) surveillance is important to get insight into the burden of disease and epidemic pattern of RSV infection. This information is useful for healthcare resource allocation as well as the timing of preventive messages and palivizumab prophylaxis. For influenza surveillance the European Influenza Surveillance Scheme (EISS) was established in 1996, but no surveillance platform is available for RSV. To improve surveillance an RSV Task Group was established in 2003 and recommendations for RSV surveillance were developed. By 2008, progress was made for four out of six recommendations: the number of European countries testing specimens for RSV increased from six to fourteen; nose and/or throat swabs were generally used for detection of influenza and RSV; a total of 25 laboratories performed molecular testing for diagnosis and participated in a quality control assessment for RSV with an overall good performance; four of the ten countries that joined EISS in 2004 started reporting RSV detections in addition to influenza in the period 2004-8. Limited progress was achieved for standardising methods and the development of a sentinel surveillance system of representative hospitals. Improving RSV surveillance is possible by further harmonising the data collection and increased reporting of RSV.
Abnormal Propagation of Calcium Waves and Ultrastructural Remodeling in Recessive Catecholaminergic Polymorphic Ventricular Tachycardia
Authors: Nian Liu, Marco Denegri, Wen Dun, Simona Boncompagni, Francesco Lodola, Feliciano Protasi, Carlo Napolitano, Penelope A. Boyden, Silvia G. Priori
Journal: Circulation Research (2013)

Rationale: The recessive form of catecholaminergic polymorphic ventricular tachycardia is caused by mutations in the cardiac calsequestrin-2 gene; this variant of catecholaminergic polymorphic ventricular tachycardia is less well characterized than the autosomal-dominant form caused by mutations in the ryanodine receptor-2 gene. Objective: We characterized the intracellular Ca 2+ homeostasis, electrophysiological properties, and ultrastructural features of the Ca 2+ release units in the homozygous calsequestrin 2-R33Q knock-in mouse model (R33Q) R33Q knock-in mouse model. Methods and Results: We studied isolated R33Q and wild-type ventricular myocytes and observed properties not previously identified in a catecholaminergic polymorphic ventricular tachycardia model. As compared with wild-type cells, R33Q myocytes (1) show spontaneous Ca 2+ waves unable to propagate as cell-wide waves; (2) show smaller Ca 2+ sparks with shortened coupling intervals, suggesting a reduced refractoriness of Ca 2+ release events; (3) have a reduction of the area of membrane contact, of the junctions between junctional sarcoplasmic reticulum and T tubules (couplons), and of junctional sarcoplasmic reticulum volume; (4) have a propensity to develop phase 2 to 4 afterdepolarizations that can elicit triggered beats; and (5) involve viral gene transfer with wild-type cardiac calsequestrin-2 that is able to normalize structural abnormalities and to restore cell-wide calcium wave propagation. Conclusions: Our data show that homozygous cardiac calsequestrin-2–R33Q myocytes develop spontaneous Ca 2+ release events with a broad range of intervals coupled to preceding beats, leading to the formation of early and delayed afterdepolarizations. They also display a major disruption of the Ca 2+ release unit architecture that leads to fragmentation of spontaneous Ca 2+ waves. We propose that these 2 substrates in R33Q myocytes synergize to provide a new arrhythmogenic mechanism for catecholaminergic polymorphic ventricular tachycardia.
Inferior Vena Cava Interruption: How and When?
Authors: Philippe Girard, Bernard Tardy, Hervé Decousus
Journal: Annual Review of Medicine (2000)

Interruption of the inferior vena cava (IVC) to prevent pulmonary embolism arising from venous thrombi in the lower extremities has become widely used since IVC filters became available about 30 years ago. However, reliable data regarding efficacy and safety of IVC filters are still lacking. The first controlled clinical trial of IVC filters demonstrated their effectiveness, but filters had no detectable impact on mortality and were associated with an increased risk of recurrent deep venous thrombosis. On the basis of the literature, indications for IVC interruption can be classified as accepted, debated, and debatable. The relevance of debated indications, more accurate identification of patients who remain “very high-risk” despite preventive or curative anticoagulant treatment, and selection of the most appropriate filter should be looked at in prospective clinical studies.
The safety profile of ustekinumab in the treatment of patients with psoriasis and concurrent hepatitis B or C
Authors: H.-Y. Chiu, C.-H. Chen, M.-S. Wu, Y.-P. Cheng, T.-F. Tsai
Journal: British Journal of Dermatology (2013)

Ustekinumab, an interleukin (IL)-12 and IL-23 blocker, has emerged as a new therapeutic option for patients with psoriasis. It is generally well tolerated but safety data on the use of ustekinumab in patients with viral hepatitis are limited.To assess the safety profile of ustekinumab in the treatment of patients with psoriasis who have concomitant hepatitis B or hepatitis C.This study included 18 patients with concurrent psoriasis and hepatitis B virus (HBV) infection (14 patients) or hepatitis C virus (HCV) infection (four patients) who were treated with at least two ustekinumab injections. Viral loads were measured at baseline and each time before the administration of ustekinumab. Relevant clinical data were recorded.Among 11 patients positive for hepatitis B surface antigen (HBsAg), two out of the seven (29%) patients who did not receive antiviral prophylaxis exhibited HBV reactivation during ustekinumab treatment. No viral reactivation was observed in the three occult HBV-infected patients (HBsAg-negative/hepatitis B core antibody-positive patients). One patient with HCV, liver cirrhosis and treated hepatocellular carcinoma (HCC) experienced HCV reactivation and recurrent HCC during the ustekinumab treatment. No significant increase in aminotransferase levels was observed in any patient.Antiviral prophylaxis appears to minimize the risk of viral reactivation in patients with concurrent psoriasis and HBV infection. Without effective anti-viral prophylaxis, the risk/benefit of ustekinumab treatment should be carefully assessed in patients with psoriasis and HBV or HCV infection and/or HCC. Close monitoring for HBV and HCV viral load is recommended, particularly for patients with high-risk factors. Serum aminotransferase determination may not be useful for early detection of viral reactivation.
P13.05 * SECOND RADIOTHERAPY TREATMENT IN RECURRENT BRAIN TUMORS
Authors: D. M. Cernea, S. Halasag, R. Stahiescu, N. Todor, S. Florian, V. I. Cernea
Journal: Neuro-Oncology (2014)

BACKGROUND: Radiotherapy for recurrent irradiated brain tumors is limited by toxicity. The purpose of this study is to determine whether second radiotherapy treatment is beneficial or not for patients with recurrent brain tumors. PATIENTS AND METHODS: In a prospective study, 11 patients who recurred after primary brain tumors, first treated between 2005-2012, were analyzed for second radiotherapy treatment. Tumor histologic types are: glioblastoma multiforme (7), grade 2 astrocytoma (2), grade 3 oligodendroglioma (1) and grade 3 oligoastrocytoma (1). First radiotherapy (RT1) was performed with TD= 50-60Gy, 2Gy/ fraction for 8 patients and TD = 30 GY, 3Gy/ fraction in one patient. DFS (disease free survival) until the recurrence was 5.3-90.6 months. Second radiotherapy treatment (RT2) was associated with surgery and chemotherapy in 8 patients, with surgery or chemotherapy 2 patients; radiotherapy alone was performed in one patient. Karnofsky Index (KI) at RT2 was >70 for 9 patients and <70 for 2 patients. RT2 was delivered with: TD = 44-10 Gy, 2 Gy/fraction, 8 patients; TD = 30-44 Gy, 2,66-3 Gy/ fraction, 3 patients. Site of recurrence, isodose distributions, PTV1 (RT1) and PTV2 (RT2), KI at the beginning and at the end of radiotherapy were compared. RESULTS: The sites of recurrences were: central and marginal, 7 patients, at distance 4 patients. The same volume was second irradiated in 4 patients. PTV2 was greater than PTV1 only for 3 patients. KI was unchanged at the end of RT2 for 10 patients. Deterioration was observed in one patient. The median follow-up was 9,22 months (5,8-20,6 months). Six patients are alive, and 5 are dead. The median follow-up was 9.22 months. CONCLUSION: There are few therapeutic options for patients with recurrent brain tumors. Regardless of histology, second radiotherapy could be one of these options alone or with other treatment methods for patients with good KI, surgery at time of recurrence and longer DFS from first treatment.
Not in front of the children
Authors: P. O'Donnell
Journal: BMJ (2001)

My father was Irish, from Cork, and came to Britain in the late 1940s. He kept in touch with events at home by way of a subscription to a Cork local newspaper, the Cork Weekly Examiner . Some of my earliest childhood memories are of him sitting in “his” armchair on a Friday night catching up on events from home.

He particularly liked to read the …
Chronic Obstructive Pulmonary Disease, Pollution, Pulmonary Vascular Disease, Transplantation, Pleural Disease, and Lung Cancer in <i>AJRCCM</i> 2000
Authors: MARTIN J. TOBIN
Journal: American Journal of Respiratory and Critical Care Medicine (2001)

1 -Antrypsin Deficiency (1) Risk Factors (7) Cellular, Molecular, and Anatomic Abnormalities (7) Lung Inflammation (7) Exhaled Markers (2) Nitric Oxide (1) Other Markers (1) Pathophysiology, Radiology, and Airway Narrowing (8) Pulmonary Vasculature (1) Control of Breathing and Exercise (9) Respiratory Muscles (3) Peripheral Muscles (3) Nutritional Status (3) Health Care Delivery (2) Drug Therapy (9) -Agonists (3) Glucocorticoids (5) Smoking Cessation (1) Other Therapies (9) Lung Volume Reduction Surgery (8) Expectorants and Mucociliary Clearance (1) Rehabilitation and Oxygen Therapy (1) Outcome (2) Air Pollution (19) General (11) Ozone (5) Diesel Exhaust (2) Environmental Tobacco Smoke (1) Pulmonary Vascular and Related Disorders (24) Pulmonary Hypertension (18) Secondary Pulmonary Hypertension (3) Molecular and Pathophysiologic Mechanisms (11) Treatment (4) Thromboembolic Disorders (2) Diagnostic Studies (1) Molecular and Pathophysiologic Mechanisms (1) High Altitude (1) Sickle Cell Disease (3) Lung Transplantation (13) Lung Preservation (2) Patient Selection (1) Obliterative Bronchiolitis (4) Animal Models (2) Cellular and Molecular Mechanisms (1) Early Detection (1) Rejection (3) Immunology and Biochemistry (1) In Cystic Fibrosis (2) Pleural Disorders (2) Diagnostic Techniques (1) Pleurodesis (1) Lung Cancer (4) Diagnosis (3) Molecular Mechanisms (1)
Tube Travel: The Role of Proteases in Individual and Collective Cancer Cell Invasion
Authors: Peter Friedl, Katarina Wolf
Journal: Cancer Research (2008)

Recent advances in high-resolution multimodal microscopy reveal how MT1-matrix metalloproteinase (MMP)/MMP-14 and other cell surface proteases degrade and remodel the extracellular matrix (ECM) to drive the dissemination of cancer cells into normal adjacent tissue. By cleaving collagen fibers and repatterning them into parallel bundles, individual cells reorient the ECM to permit movement in tube-like microtracks. Cells along the edge of these tubes can excavate ECM outward, generating macrotracks through which collective mass movement of cancer cells can occur. These findings develop our understanding of invasive processes in cancer and how to attack them by interfering with MMP-14 activity.
Total energy expenditure in children with obstructive sleep apnoea syndrome
Authors: R.M. Bland, S. Bulgarelli, J.C. Ventham, D. Jackson, J.J. Reilly, J.Y. Paton
Journal: European Respiratory Journal (2001)

Childhood obstructive sleep apnoea syndrome (OSAS) acts as a check on growth and nutritional status. An increase in sleeping energy expenditure has been proposed as a possible mechanism, but to date, no studies have determined whether energy requirements (total energy expenditure; TEE) are raised in OSAS. The aim of this study was to test the hypothesis that OSAS is associated with increased TEE. Eleven children (mean±sd 5.8±2.2 yrs of age) with OSAS confirmed by nocturnal polysomnography were each matched with a pair of healthy controls (n=22) of the same age and sex. TEE was measured using the doubly-labelled water method in all subjects. In 10/11 patients TEE was also measured after adenotonsillectomy and changes in TEE assessed. There was no significant difference in TEE between patients (mean±sd 325±44 kJ·kg −1 ·day −1 ) and controls (339±48 kJ·kg −1 ·day −1 ), nor between patients and age- and sex-specific literature data on TEE, using the doubly-labelled water method. Differences in TEE within patients, before versus after surgery, were minor and not statistically significant. This study does not support the hypothesis that obstructive sleep apnoea syndrome in childhood is associated with increased energy requirements, and suggests that alternative explanations for the effect of this syndrome on growth and energy balance should be sought.
CRISPR-Cas systems target a diverse collection of invasive mobile genetic elements in human microbiomes
Authors: Quan Zhang, Mina Rho, Haixu Tang, Thomas G Doak, Yuzhen Ye
Journal: Genome biology (2013)

Abstract Background Bacteria and archaea develop immunity against invading genomes by incorporating pieces of the invaders' sequences, called spacers, into a clustered regularly interspaced short palindromic repeats (CRISPR) locus between repeats, forming arrays of repeat-spacer units. When spacers are expressed, they direct CRISPR-associated (Cas) proteins to silence complementary invading DNA. In order to characterize the invaders of human microbiomes, we use spacers from CRISPR arrays that we had previously assembled from shotgun metagenomic datasets, and identify contigs that contain these spacers' targets. Results We discover 95,000 contigs that are putative invasive mobile genetic elements, some targeted by hundreds of CRISPR spacers. We find that oral sites in healthy human populations have a much greater variety of mobile genetic elements than stool samples. Mobile genetic elements carry genes encoding diverse functions: only 7% of the mobile genetic elements are similar to known phages or plasmids, although a much greater proportion contain phage- or plasmid-related genes. A small number of contigs share similarity with known integrative and conjugative elements, providing the first examples of CRISPR defenses against this class of element. We provide detailed analyses of a few large mobile genetic elements of various types, and a relative abundance analysis of mobile genetic elements and putative hosts, exploring the dynamic activities of mobile genetic elements in human microbiomes. A joint analysis of mobile genetic elements and CRISPRs shows that protospacer-adjacent motifs drive their interaction network; however, some CRISPR-Cas systems target mobile genetic elements lacking motifs. Conclusions We identify a large collection of invasive mobile genetic elements in human microbiomes, an important resource for further study of the interaction between the CRISPR-Cas immune system and invaders.