tbuckley/cabot-search huggingface dataset:
Michael Lee-Jones
Authors: P. Kay
Journal: BMJ (2003)

Former general practitioner Wallingford, Oxfordshire (b London 1937; q Middlesex Hospital, London, 1960; MRCP, FRCGP), died from lung cancer on 9 November 2002.

Mike joined a well established general practice in Wallingford in 1971. He had a special interest in obstetrics, taking an active part in deliveries at home or in the local community hospital. Mike was one of a small team that introduced new operational policies for Wallingford Community Hospital. From 1992 he was involved in the hospital accreditation programme and after retirement from general practice in 1998 he became the programme's clinical director for three years. Music, the theatre, and sailing were among Mike's many interests. He leaves a wife, Belinda, and three children.
Obesity increases risk of several cancers in men and women, study finds
Authors: Roger Dobson
Journal: BMJ (2005)

Being overweight or obese increases the risk of several cancers in men and women, a new study has found.

The research, which followed more than 145 000 people in Austria for 10 years, shows that high body weight was associated with a greater risk of colon, rectal, and pancreatic cancer in men and of endometrial and non-Hodgkin's lymphomas in women ( British Journal of Cancer 2005;93:1062-7).

A high body mass index (BMI) also seemed to increase the risk of breast cancer among women aged 65 or more.

“Our study provides additional …
Long-Term Effects of Inhaled Corticosteroids on FEV<sub>1</sub> in Patients with Chronic Obstructive Pulmonary Disease
Authors: Kristin B. Highland, Charlie Strange, John E. Heffner
Journal: Annals of Internal Medicine (2003)

Background: There is no consensus on the effectiveness of inhaled corticosteroids for the treatment of chronic obstructive pulmonary disease (COPD). Purpose: To evaluate the long-term effects of inhaled corticosteroids on the rate of FEV1 decline in patients with COPD. Data Sources: MEDLINE, EMBASE, CISCOM, and AMED databases and the Cochrane Library (1966 to December 2002), reference lists from identified articles, and consultation with experts. Searches were not limited to the English language. Study Selection: Randomized, placebo-controlled trials that examined the rate of FEV1 decline as a primary outcome in patients with COPD. Data Extraction: Two reviewers independently extracted the data by using predetermined criteria. Data Synthesis: For the six studies that met the inclusion criteria, the summary estimate for the difference in FEV1 decline between the placebo and treatment groups was 5.0 3.2 mL/y (95% CI, 11.2 to 1.2 mL/y; P = 0.11). Conclusions: The use of inhaled corticosteroids was not associated with the rate of FEV1 decline in 3571 patients followed for 24 to 54 months.
Cytotoxic T cell response against the chimeric ETV6-AML1 protein in childhood acute lymphoblastic leukemia.
Authors: P Yotnda, F Garcia, M Peuchmaur, B Grandchamp, M Duval, F Lemonnier, E Vilmer, P Langlade-Demoyen
Journal: Journal of Clinical Investigation (1998)

Cytotoxic T lymphocytes (CTL) are potent effector cells that could provide long term antitumor immunity if induced by appropriate vaccines. CTL recognize 8-14 amino acid-long peptides processed intracellularly and presented by MHC class I molecules. A well-characterized example of a potential tumor antigen in childhood pre-B Acute Lymphoblastic Leukemia (ALL) results from the chromosomal translocation 12;21 leading to the fusion of the ETV6 and AML1 genes. This translocation is observed in > 25% of ALL-patients. In this study, we have examined whether the chimeric ETV6-AML1 protein could serve as a tumor specific antigen for CTL in HLA-A2.1 individuals. We have identified a nonapeptide (RIAECILGM), encoded by the fusion region of the ETV6-AML1 protein, that binds to HLA-A2.1 molecules and induces specific primary CTL in peripheral blood lymphocytes from healthy donors. These CTL specifically lysed HLA-A2.1 tumor cells endogeneously expressing the ETV6-AML fusion protein. CTL with similar functional capacities were found with high frequencies and cloned from one patient's bone marrow indicating that ETV6-AML1-specific anti-ALL CTL are, at least in some patients, spontaneously stimulated and might participate to host antileukemia defense.
A switch to endoscopic mucosal resection after precutting following gastric perforation during endoscopic submucosal dissection: a simple and useful technique
Authors: D. Lee, H. Lee, M. Jung, S. Kim, S. Jeon
Journal: Endoscopy (2012)

Endoscopic submucosal dissection (ESD) is safe and effective, but as the number of patients undergoing ESD has increased, so has the number of iatrogenic perforations. We describe the effectiveness and benefits of endoscopic mucosal resection after precutting (EMR-P) in a series of patients who developed a macroperforation during ESD. This was a retrospective, single-center case series from a prospectively maintained database in an academic tertiary care center. The study involved 16 patients with macroperforation out of 1171 patients who underwent ESD between November 2006 and January 2011. En bloc resection by EMR-P was achieved in 12 out of 16 patients (75 %) and piecemeal resection in 4 (25 %). All patients were discharged after a mean hospital stay of 6.8 days without further complications. There were no recurrences during the median follow-up period of 11.4 months. Macroperforation during ESD can be managed successfully by endoscopic closure, and EMR-P should then be considered.
A Comparative Family Study of Rheumatoid Arthritis and Systemic Lupus Erythematosus
Authors: M. Siegel, S. L. Lee, D. Widelock, N. V. Gwon, H. Kravitz
Journal: New England Journal of Medicine (1965)

CONFLICTING results have been reported recently on the occurrence of serologic and physical abnormalities in families with a case of collagen disease. Most reports in the past fifteen years have described a high frequency of arthritic and serologic abnormalities characteristic of the collagen diseases among relatives of patients with rheumatoid arthritis or systemic lupus erythematosus.1 , 2 In a few reports on systemic lupus erythematosus, however, the increase above normal expectancy was not marked.3 , 4 And in some recent studies on rheumatoid arthritis no evidence of a familial aggregation of the disease was reported.5 6 7 These variations in results reflect differences in study design . . .
IL-2 induces a WAVE2-dependent pathway for actin reorganization that enables WASp-independent human NK cell function
Authors: Jordan S. Orange, Sumita Roy-Ghanta, Emily M. Mace, Saumya Maru, Gregory D. Rak, Keri B. Sanborn, Anders Fasth, Rushani Saltzman, Allison Paisley, Linda Monaco-Shawver, Pinaki P. Banerjee, Rahul Pandey
Journal: Journal of Clinical Investigation (2011)

Wiskott-Aldrich syndrome (WAS) is a primary immunodeficiency associated with an increased susceptibility to herpesvirus infection and hematologic malignancy as well as a deficiency of NK cell function. It is caused by defective WAS protein (WASp). WASp facilitates filamentous actin (F-actin) branching and is required for F-actin accumulation at the NK cell immunological synapse and NK cell cytotoxicity ex vivo. Importantly, the function of WASp-deficient NK cells can be restored in vitro after exposure to IL-2, but the mechanisms underlying this remain unknown. Using a WASp inhibitor as well as cells from patients with WAS, we have defined a direct effect of IL-2 signaling upon F-actin that is independent of WASp function. We found that IL-2 treatment of a patient with WAS enhanced the cytotoxicity of their NK cells and the F-actin content at the immunological synapses formed by their NK cells. IL-2 stimulation of NK cells in vitro activated the WASp homolog WAVE2, which was required for inducing WASp-independent NK cell function, but not for baseline activity. Thus, WAVE2 and WASp define parallel pathways to F-actin reorganization and function in human NK cells; although WAVE2 was not required for NK cell innate function, it was accessible through adaptive immunity via IL-2. These results demonstrate how overlapping cytoskeletal activities can utilize immunologically distinct pathways to achieve synonymous immune function.
Book Review Minority Health in America: Findings and policy implications from the Commonwealth Fund Minority Health Survey Edited by Carol J. Hogue, Martha A. Hargraves, and Karen Scott Collins. 344 pp. Baltimore, Johns Hopkins University Press, 2000. $22.50 (paper); $49.95 (cloth). 0-8018-6299-X (paper); 0-8018-6298-1 (cloth).
Authors: J. Tyson Tildon
Journal: New England Journal of Medicine (2000)
Novel Gene Locus for Autosomal Dominant Left Ventricular Noncompaction Maps to Chromosome 11p15
Authors: Sabine Sasse-Klaassen, Susanne Probst, Brenda Gerull, Erwin Oechslin, Peter Nürnberg, Arnd Heuser, Rolf Jenni, Hans Christian Hennies, Ludwig Thierfelder
Journal: Circulation (2004)

Left ventricular noncompaction (LVNC) is a congenital unclassified cardiomyopathy with numerous prominent trabeculations and deep intertrabecular recesses in a hypertrophied and hypokinetic myocardium. It has been reported to occur in isolation or in association with congenital heart disease. Mutations in the X-linked G4.5 gene are responsible for cases of isolated LVNC in male infants, but G4.5 mutations were not found in patients with clinical onset of disease in adulthood. In addition, several families with LVNC and an autosomal dominant pattern of inheritance suggest genetic heterogeneity.We performed a genome-wide linkage analysis in a family with autosomal dominant LVNC and show that a locus containing the LVNC disease gene maps to chromosome 11p15. A peak 2-point logarithm of odds score of 5.06 was obtained with marker D11S902 at theta=0. Haplotype analysis defined a critical interval of 6.4 centimorgan between D11S1794 and D11S928 corresponding to a physical distance of 6.8 megabases. No disease-causing mutation was identified in 2 prime positional candidate genes, muscle LIM protein (MLP) and SOX6.We have mapped a locus for autosomal dominant LVNC to a 6.8-megabase region on human chromosome 11p15. Identification of the disease gene will allow genetic screening and provide fundamental insight into the understanding of myocardial morphogenesis.
Persistent Hyperreactivity and Reactive Airway Dysfunction in Firefighters at the World Trade Center
Authors: Gisela I. Banauch, Dawn Alleyne, Raoul Sanchez, Kattia Olender, Hillel W. Cohen, Michael Weiden, Kerry J. Kelly, David J. Prezant
Journal: American Journal of Respiratory and Critical Care Medicine (2003)

New York City Fire Department rescue workers experienced massive exposure to airborne particulates at the World Trade Center site. Aims of this longitudinal study were to (1) determine if bronchial hyperreactivity was present, persistent, and independently associated with exposure intensity, (2) identify objective measures shortly after the collapse that would predict persistent hyperreactivity and a diagnosis of reactive airways dysfunction 6 months post-collapse. A representative sample of 179 rescue workers stratified by exposure intensity (high, moderate, and control) without current smoking or prior respiratory disease was enrolled. Highly exposed workers arrived within 2 hours of collapse, moderately exposed workers arrived later on Days 1-2; control subjects were not exposed. Hyperreactivity at 1, 3, and 6 months post-collapse was associated with exposure intensity, independent of ex-smoking and airflow obstruction. Six months post-collapse, highly exposed workers were 6.8 times more likely than moderately exposed workers and control subjects to be hyperreactive (95% confidence interval, 1.8-25.2; p = 0.004), and hyperreactivity persisted in 55% of those hyperreactive at 1 and/or 3 months. In highly exposed subjects, hyperreactivity 1 or 3 months post-collapse was the sole predictor for reactive airways dysfunction (p = 0.021). In conclusion, development and persistence of hyperreactivity and reactive airways dysfunction were strongly and independently associated with exposure intensity. Hyperreactivity shortly post-collapse predicted reactive airways dysfunction at 6 months in highly exposed workers; this has important implications for disaster management.
Monocyte chemoattractant protein-1 plasma level is elevated in patients with compensated ischemic cardiomyopathy but not the tumor necrosis factor-alpha
Authors: Samer J. Khouri, Jeanette Pohorence Ferguson, Laura Yamokoski, Karen Donavan, Amy Ferketich, Philip Binkley
Journal: Journal of the American College of Cardiology (2003)
Killing the primary heart pacemaker
Authors: M. E. Mangoni
Journal: Cardiovascular Research (2011)

This editorial refers to ‘Insights into sick sinus syndrome from an inducible mouse model’ by S. Herrmann et al. , pp. 38–48, this issue. 

The most aggressive reviewer I have ever experienced is my barber. When I first came into his shop, conviviality naturally drove the conversation towards my job. Once asked about my research field I proudly replied: ‘I work on the mechanisms underlying the genesis and regulation of the heartbeat'. He looked surprised that such an important and apparently self-evident physiological function was still enveloped by some kind of uncertainty. ‘I am amazed that we are still paying researchers with public money to work on such an obvious thing'. To demonstrate that we still deserve our salaries, I explained that, while potentially counterintuitive, cardiac pacemaking is a complex function and several aspects of how heart rate is determined at the cellular and tissue level are not completely understood. Hermann et al .1 will further fuel the current debate on cardiac automaticity (and accessorily my personal debate with the barber).

Heart pacemaker activity is generated in the sino-atrial node (SAN) by a relatively small population of specialized automatic myocytes. Beside the SAN, the atrioventricular node (AVN) and the Purkinje fibres network also contain spontaneously active myocytes. However, since the SAN possesses the highest intrinsic rate of pacing, it determines the heart rate under physiological conditions and constitutes the ‘primary’ cardiac rhythmogenic centre. …
B-1 B Cell Development in the Fetus and Adult
Authors: Encarnacion Montecino-Rodriguez, Kenneth Dorshkind
Journal: Immunity (2012)

Models of hematopoiesis often depict lymphocyte production as a uniform process in which a homogenous population of hematopoietic stem cells (HSCs) generates progenitors from which all types of lymphocytes are derived. However, it is increasingly evident that these schemes are too simplistic and that the lymphoid potential of HSCs and precursors arising in the embryo, fetus, neonate, and adult is remarkably distinct. We review recent findings regarding the development of B lymphocytes, and the B-1 B cell lineage in particular, as a case in point. These studies show that B-1 and B-2 B cells involved in innate and adaptive immune responses, respectively, arise in staggered waves of development from distinct progenitors. We discuss the implications of this layered model of B cell development for understanding normal and dysregulated B lymphopoiesis. Models of hematopoiesis often depict lymphocyte production as a uniform process in which a homogenous population of hematopoietic stem cells (HSCs) generates progenitors from which all types of lymphocytes are derived. However, it is increasingly evident that these schemes are too simplistic and that the lymphoid potential of HSCs and precursors arising in the embryo, fetus, neonate, and adult is remarkably distinct. We review recent findings regarding the development of B lymphocytes, and the B-1 B cell lineage in particular, as a case in point. These studies show that B-1 and B-2 B cells involved in innate and adaptive immune responses, respectively, arise in staggered waves of development from distinct progenitors. We discuss the implications of this layered model of B cell development for understanding normal and dysregulated B lymphopoiesis.
Doctors forced to guard Baghdad hospitals after looting
Authors: O. Dyer
Journal: BMJ (2003)

At least one Baghdad hospital has been completely ransacked in looting sparked off by the arrival of American forces in the city. Some hospitals were being guarded by medical staff with guns; others were largely abandoned as staff tried to protect their homes.

The al-Kindi Hospital was left bare of equipment, according to staff of the International Committee of the Red Cross. The Yarmouk Hospital was damaged and looted.

As the BMJ went to press, the International Committee of the Red Cross was still unsure how many …
Association of Graves' Disease With Turner's Syndrome
Authors: Takeki Hirano
Journal: JAMA (1981)

<h3>To the Editor.—</h3> An increased incidence of thyroid autoantibodies is known to occur in patients with Turner's syndrome.<sup>1,2</sup>The disorders closely related to thyroid autoantibodies are Hashimoto's disease and Graves' disease. A striking association of Hashimoto's disease with Turner's syndrome, especially due to structural variations of an X chromosome, has been repeatedly shown.<sup>1-4</sup>Yet, Graves' disease has rarely been documented in patients with this chromosomal abnormality.<sup>4</sup> <h3>Report of a Case.—</h3> When this woman was born, a karyotype of 45,XO (Turner's syndrome) was determined during the investigation of bilateral pedal edema. The physical findings included hypertelorism, slight cubitus valgus, and a widely spaced nipple. A webbed neck, a low hairline, and multiple, pigmented nevi were absent. At age 11 years, because of the absence of secondary sex characteristics, she was given a conjugated estrogen preparation for two years, followed by the addition of medroxyprogesterone for the onset of
Site of the abnormal stimulus of gastric secretion after small bowel exclusion
Authors: B. Buxton, A. E. O. Wasunna, J. Saunders, I. E. Gillespie
Journal: Gut (1972)

In dogs with either vagally innervated or denervated pouches, the acid responses to a standard meal, a meal which bypassed the greater part of the small bowel, and a meal introduced directly into the small intestine were measured before and after exclusion of 75% of the small bowel. After intestinal exclusion an increase in acid secretion was found in the latter part of the acid response to the standard meal and the intestinal meal. No increase in acid secretion resulted from the meals which bypassed the small bowel. These findings suggest that an increase in stimulation from the remaining small intestine is responsible for the elevation in acid secretion following small bowel exclusion.
Interleukin-4 therapy of psoriasis induces Th2 responses and improves human autoimmune disease
Authors: Kamran Ghoreschi, Peter Thomas, Susanne Breit, Martin Dugas, Reinhard Mailhammer, Willem van Eden, Ruurd van der Zee, Tilo Biedermann, Jörg Prinz, Matthias Mack, Ulrich Mrowietz, Enno Christophers, Detlef Schlöndorff, Gerd Plewig, Christian A. Sander, Martin Röcken
Journal: Nature Medicine (2002)
Greenfield Filter vs Mobin-Uddin Umbrella
Authors: George E. Cimochowski
Journal: JAMA (1980)

<h3>To the Editor.—</h3> Recently Scott et al (1980;243:1133) described a new complication for the Mobin-Uddin umbrella—a septic clot in a thrombosed Mobin-Uddin umbrella. This required therapy with a general anesthetic and surgical removal of the clot and umbrella; the clot when cultured grew<i>Staphylococcus aureus</i>coagulase-positive bacteria. Again, we believe that this is further evidence why the Greenfield filter is a superior device to interrupt the vena cava. As we reported recently,<sup>1</sup>the Greenfield filter not only has the same recurrent minimal embolic rate as the Mobin-Uddin, but it surpasses the Mobin-Uddin in ease of insertion because of the ability to pass it either transfemorally or transjugularly. Most importantly, it is designed to remain patent and in fact does remain patent, as we reported a long-term patency rate of 98%. We believe that the use of the Mobin-Uddin umbrella with its inherent design to clot could lead to the
We risk forgetting what it means to be free
Authors: Lesley Morrison
Journal: BMJ (2006)

<h3>ABSTRACT</h3> <h3>Introduction</h3> Tocilizumab is an anti-interleukin-6 antibody that has been used for the treatment of severe coronavirus disease 2019 (COVID-19). However, the concrete evidence of its benefit in reducing the mortality in severe COVID-19 is lacking. Therefore, we performed a systematic review and meta-analysis of relevant studies that compared the efficacy of Tocilizumab in severe COVID-19 vs. standard of care alone. <h3>Methods</h3> Literature search for studies that compared ‘Tocilizumab’ and ‘Standard of care’ in the treatment of COVID-19 was done using major online databases from December 2019 to June 14<sup>th</sup>, 2020. Search words ‘ Tocilizumab,’ ‘anti-interleukin-6 antibody,’ and ‘COVID-19’ or ‘coronavirus 2019’ in various combinations were used. Articles in the form of abstracts, letters without original data, case reports, and reviews were excluded. Data was gathered on an excel sheet, and statistical analysis was performed using Review Manager 5.3. <h3>Results</h3> Sixteen studies were eligible from 693 initial studies, including 3,641 patients (64% males). There were thirteen retrospective studies and three prospective studies. There were 2,488 patients in the standard of care group (61.7%) and 1,153 patients (68.7%) in the Tocilizumab group. The death rate in the tocilizumab group, 22.4% (258/1153), was lower than the standard of care group, 26.21% (652/2,488) (Pooled odds ratio 0.57 [95% CI 0.36-0.92] p=0.02). There was a significant heterogeneity (Inconsistency index= 80%) among the included studies. <h3>Conclusion</h3> The addition of Tocilizumab to the standard of care might reduce the mortality in severe COVID-19. Larger randomized clinical trials are needed to validate these findings.
Relations among sodium pump inhibition, Na-Ca and Na-H exchange activities, and Ca-H interaction in cultured chick heart cells.
Authors: D Kim, E J Cragoe, T W Smith
Journal: Circulation Research (1987)

Sodium pump inhibition in cardiac muscle cells is associated with changes in intracellular sodium, calcium, and hydrogen concentrations as well as in membrane ion transport activity. We examined further the functional relations among these entities using cultured chick ventricular cells. [Ca]i and pHi were determined from fluorescence signals obtained from cells loaded with fura-2 or BCECF, respectively. Ouabain (100 microM) elevated [Ca]i eightfold and decreased pHi by 0.11 unit (a 30% increase in [H+]). In the presence of 10 microM ethylisopropylamiloride, a potent inhibitor of Na-H exchange, ouabain elevated [Ca]i 3.5-fold and reduced pHi by 0.16 unit (a 48% increase in [H+]). Exposure to sodium-free (sodium replaced with potassium) medium produced a twelvefold increase in [Ca]i and a 0.12 pH unit decrease in pHi. In cells treated with 100 microM ouabain, exposure to sodium-free (lithium) medium resulted in a 22-fold sustained increase in [Ca]i and a rapid intracellular acidification (pH 7.15 to 6.60). The effect of ouabain or sodium-free medium on pHi was abolished in calcium-free medium; addition of 1 mM Ca rapidly increased [Ca]i and decreased pHi. In cells treated with subtoxic (3 microM) or toxic (100 microM) concentrations of ouabain, initial 24Na uptake rates were significantly greater than in control cells and were significantly reduced in the presence of 10 microM ethylisopropylamiloride. We conclude that ouabain (100 microM) produces intracellular acidification as a result of sodium pump inhibition; calcium accumulation via Na-Ca exchange, and subsequent Ca-H interaction within the cell.(ABSTRACT TRUNCATED AT 250 WORDS)