tbuckley/cabot-search huggingface dataset:
Complete Occlusion of the Superior Vena Cava with Chronic Mediastinitis in a Case of Generalized Actinomycosis
Authors: J. P. D. Mounsey
Journal: Thorax (1947)

IFor Plates see pase 1941 Ochsner and Dixon (1936), in a review of world literature, cited 120 cases of supenor vena caval thrombosis.Twenty-eight of these were due to chronic mediastinitis, of which eleven were stated to be due to syphilis, ten to tubercu- losis, one to pyogenic infection, one to trauma, and five of unknown aetiology.Tubbs (1946) reported three further cases of superior vena caval obstruction, one of which was probably due to syphilis, the remaining two being of unknown aetiology.Renbourn (1946) reported a case of superior vena caval thrombosis of unknown aetiology, with complete superior vena caval obstruction.The above authorities do not mention actinomycosis as a cause.Cope (1938) stated that " primary thoracic actinomycosis can and most likely does fairly frequently commence by the fungus penetrating the wall of the oesophagus and reaching the mediastinum."He described two main types, the pulmonary and the mediastinal, and he discussed the general symptoms and signs of thoracic actinomycosis and its complications, but did not mention superior vena caval obstruction among these.Fischer (1904) gave actinomycosis as the cause of superior vena caval obstruction in 0.5 per cent of cases, but I was unable to trace a copy of this work.Nor was I able to find, in the literature available, any other reported cases of superior vena caval occlusion with chronic mediastinitis due to actinomycosis. CASE REPORTA man, aged 43, whose occupation was parcel clerk, was referred to hospital with a diagnosis of mediastinal abscess.PAST HISTORY.-Hishistory was characterized by its chronicity and diversity, pointing to the involvement of many systems.For five to ten years before admission the patient had been known to have had tachycardia and a dry unproductive cough.During the last two years he had been under observation, and his case was considered at different times to be suggestive of tuberculosis, thyrotoxicosis, and pulmonary or mediastinal new growth.Investigations, which included sputum examination, gland biopsy, and bronchoscopy, failed on July 21,
Endothelin inhibits fluid and bicarbonate transport in part by reducing Na+/K+ ATPase activity in the rat proximal straight tubule.
Authors: J Garvin, K Sanders
Journal: Journal of the American Society of Nephrology (1991)

The effects of endothelin on fluid and bicarbonate absorption and Na+/K+ ATPase activity in the proximal straight tubule were investigated. During the control period, fluid absorption was 0.59 +/- 0.03 nL/mm.min when tubules were perfused at 4.76 nL/mm.min. After treatment with 10(-9) M endothelin, fluid absorption fell to 0.36 +/- 0.06 nL/mm.min when perfused at a similar flow rate. During the control period, bicarbonate absorption was 67.9 +/- 3.6 pmol/mm.min. After treatment with endothelin, it fell to 42.8 +/- 4.3 pmol/mm.min, an inhibition of 38%. To test whether inhibition of fluid and bicarbonate absorption was due to suppression of Na+/K+ ATPase activity, the effect of endothelin on pump activity was investigated. In control tubules, Na+/K+ ATPase activity was 85 +/- 5 pmol/mm.min. In endothelin-treated tubules, Na+/K+ ATPase activity was 68 +/- 4 pmol/mm.min, a reduction of 20%. From these data, it was concluded that endothelin inhibits fluid and bicarbonate transport in the proximal tubule and that this inhibition is in part due to suppression of Na+/K+ ATPase activity.
Mitochondrial Cardioencephalomyopathy Due to a Novel SCO2 Mutation in a Brazilian Patient
Authors: Juliana Gurgel-Giannetti, Guilherme Oliveira, Geraldo Brasileiro Filho, Poliana Martins, Mariz Vainzof, Michio Hirano
Journal: JAMA Neurology (2012)

To review all patients with SCO2 mutations and to describe a Brazilian patient with cardioencephalomyopathy carrying compound heterozygous mutations in SCO2, one being the known pathogenic p.E140K mutation and the other a novel 12-base pair (bp) deletion at nucleotides 1519 through 1530 (c.1519_1530del).Case report and literature review.University hospital.Infant girl presenting with an encephalomyopathy, inspiratory stridor, ventilator failure, progressive hypotonia, and weakness, leading to death.Clinical features, neuroimaging findings, muscle biopsy with histochemical analysis, and genetic studies.This infant girl was the first child of healthy, nonconsanguineous parents. She developed progressive muscular hypotonia and ventilatory failure. At the end of the first month of life, she developed cardiomegaly and signs of cardiac failure. Routine blood tests showed lactic acidosis and mild elevation of the creatine kinase level. Brain magnetic resonance imaging showed increased T2 and fluid-attenuated inversion recovery signals in the putamen bilaterally. Nerve conduction studies showed severe axonal sensorimotor neuropathy. Muscle biopsy revealed a neurogenic pattern with mitochondrial proliferation and total absence of cytochrome- c oxidase histochemical stain. Sequencing of SCO2 showed that the patient had compound heterozygote SCO2 mutations: the previously described c.1541G>A (p.E140K) mutation and a novel 12-bp deletion at nucleotides 1519 through 1530 (c.1519_1530del). The patient died at age 45 days.Our findings and the literature review indicate that it is important to consider the diagnosis of mitochondrial disease in newborns with hypotonia and cardiomyopathy. In our case, the accurate diagnosis of SCO2 mutations is particularly important for genetic counseling.
There is more to biological behavior than causation and control
Authors: Mark A Krause
Journal: Behavioral and Brain Sciences (2001)

Biorobots may model the causation of relatively simple behaviors, but many animal behaviorists are concerned with complex cognitive traits and their evolution. Biorobotics seems limited in its ability to model cognition and to provide evolutionary explanations. Also, if robots could model complex traits, such as theory of mind, underdetermination could be problematic. Underdetermination is also a challenge for comparative psychologists.
Food induced stimulation of the antisecretory factor can improve symptoms in human inflammatory bowel disease: a study of a concept
Authors: S Bjorck
Journal: Gut (2000)

<h3>BACKGROUND</h3> Antisecretory factor (AF), a 41 kDa cloned and sequenced protein, suppresses intestinal inflammation and hypersecretion in animals. Endogenous AF production can be induced by dietary modifications in several animal species, and this feed has been shown to reduce the incidence of diarrhoeal disease in weaning piglets. The role of AF in intestinal disease in humans is not known. <h3>AIMS</h3> To study the effects of hydrothermally processed cereals, optimised for AF induction in animals, added to the diet of patients with longstanding symptoms of inflammatory bowel disease (IBD). <h3>PATIENTS</h3> Fifty three patients with IBD (ulcerative colitis and Crohn9s disease) were entered into the study, and 50 completed follow up. The experimental group consisted of 16 females (mean age 50 (SEM 5) years) and 10 males (41 (4) years) and the placebo group of 12 women (41 (4) years old) and 12 men (51 (5) years). <h3>METHODS</h3> Patients were randomised to receive either hydrothermally processed cereals (active treatment) or the same amount of ordinary cereals (placebo treatment) for four weeks in a double blind study design. Baseline diet and medications remained unchanged. Bowel symptoms, plasma levels of AF, and colonic biopsies were evaluated before and after treatment. <h3>RESULTS</h3> The active treatment significantly improved subjective ratings of clinical symptoms and increased plasma AF levels compared with placebo. Plasma lipid levels were unaffected. <h3>CONCLUSION</h3> Hydrothermally processed cereals can induce AF production in human IBD. This increase in endogenous AF activity is associated with clinical improvement. Further studies are warranted to clarify the exact role of AF in human intestinal disease.
The Role of Intramolecular Epitope Spreading in the Pathogenesis of Endemic Pemphigus Foliaceus (Fogo Selvagem)
Authors: Ning Li, Valeria Aoki, Gunter Hans-Filho, Evandro A. Rivitti, Luis A. Diaz
Journal: The Journal of Experimental Medicine (2003)

We report here a relationship between intramolecular epitope spreading and the clinical onset of the endemic form of pemphigus foliaceus in a Brazilian community with a high prevalence and incidence of the disease. Also known as Fogo Selvagem (FS), this disease is characterized by severe skin blistering and pathogenic anti–desmoglein-1 (Dsg1) autoantibodies. These autoantibodies bind the Dsg1 ectodomain and trigger keratinocyte cell detachment, the hallmark of FS. We show that (a) sera from FS patients in the preclinical stage recognized epitopes on the COOH-terminal EC5 domain of Dsg1, (b) disease onset was associated with the emergence of antibodies specific for epitopes on the NH2-terminal EC1 and EC2 domains, (c) all sera from FS patients with active disease recognized the EC1 and/or EC2 domains, and (d) sera from FS patients in remission showed reactivity restricted to EC5. These results suggest that anti-Dsg1 autoantibodies in FS are initially raised against the COOH-terminal EC5 domain of Dsg1 in individuals without skin disease; in genetically predisposed subjects the autoimmune response may then undergo intramolecular epitope spreading toward epitopes on the NH2-terminal EC1 and EC2 domains of Dsg1 leading to disease onset. Moreover, intramolecular epitope spreading may also modulate remissions and relapses of FS.
Racial Categories in Medical Practice: How Useful Are They?
Authors: Lundy Braun, Anne Fausto-Sterling, Duana Fullwiley, Evelynn M Hammonds, Alondra Nelson, William Quivers, Susan M Reverby, Alexandra E Shields
Journal: PLoS Medicine (2007)

research journals [10][11][12][13][14][15][16][17].Throughout the 20th century, race had no standard defi nition in medical, epidemiological, or health services research [18][19][20][21].In epidemiology, race vaguely referred to "persons who are relatively homogenous with respect to biologic inheritance" [18].One survey of medical and epidemiological
GPs should not be deterred from prescribing quinine
Authors: H A D. Ar
Journal: BMJ (1996)

EDITOR,—In their paper on the prescribing of quinine and drugs that induce cramp the authors seem to be trying to convey three messages, all in my opinion fallacious.1 One is that quinine is of doubtful efficacy in nocturnal cramps. Since Man-Son-Hing and Wells found a positive result for the drug in all of the six perfectly designed clinical trials that they analysed in their meta-analysis,2 I wonder what grounds the authors have for maintaining that …
Phase II Trial of Cetuximab in Patients With Refractory Colorectal Cancer That Expresses the Epidermal Growth Factor Receptor
Authors: Leonard B. Saltz, Neal J. Meropol, Patrick J. Loehrer, Michael N. Needle, Justin Kopit, Robert J. Mayer
Journal: Journal of Clinical Oncology (2004)

To evaluate the antitumor activity and toxicity of single-agent cetuximab in patients with chemotherapy-refractory colorectal cancer whose tumors express the epidermal growth factor receptor.Phase II, open-label clinical trial. Patients were required to have EGFr expression demonstrated on formalin-fixed paraffin-embedded tumor tissue by immunohistochemical staining before study participation. Patients were required to have received irinotecan, either alone or in a combination regimen, and to have demonstrated clinical failure on this regimen before study entry. Cetuximab was administered weekly by intravenous infusion. The first dose of 400 mg/m(2) was given during the course of 2 hours. Subsequent weekly treatments were given at a dose of 250 mg/m(2) during the course of 1 hour.Fifty-seven eligible patients were treated. All were assessable for toxicity and response. The most commonly encountered grade 3 to 4 adverse events, regardless of relationship to study drug, were an acne-like skin rash, predominantly on the face and upper torso (86% with any grade; 18% with grade 3), and a composite of asthenia, fatigue, malaise, or lethargy (56% with any grade, 9% with grade 3). Two patients (3.5%) experienced grade 3 allergic reactions requiring discontinuation of study treatment. A third patient experienced a grade 3 allergic reaction that resolved, and the patient continued on the study. Neither diarrhea nor neutropenia were dose limiting in any of the 57 patients treated. Five patients (9%; 95% CI, 3% to 19%) achieved a partial response. Twenty-one additional patients had stable disease or minor responses. The median survival in these previously treated patients with chemotherapy-refractory colorectal cancer is 6.4 months.Cetuximab on this once-weekly schedule has modest activity and is well-tolerated as a single agent in patients with chemotherapy-refractory colorectal cancer whose tumors express the epidermal growth factor receptor. Further studies of cetuximab will evaluate the use of cetuximab in conjunction with first-line and adjuvant treatments for this disease.
Pulse steroid therapy in rheumatoid arthritis: can equivalent doses of oral prednisolone give similar clinical results to intravenous methylprednisolone?
Authors: M D Smith, M J Ahern, P J Roberts-Thomson
Journal: Annals of the Rheumatic Diseases (1988)

Pulse methylprednisolone therapy has dramatic effects on clinical and immunological parameters of disease activity in patients with rheumatoid arthritis. Previous studies of this treatment have all used the intravenous route and methylprednisolone succinate. This study addresses the question of whether oral prednisolone in equivalent doses can substitute for intravenous methylprednisolone in pulse therapy in a double blind parallel study. It is shown that oral prednisolone has clinical and immunological effects equivalent to those of intravenous methylprednisolone, making it possible to administer pulse therapy to patients with rheumatoid arthritis as outpatients without the inconvenience and inherent dangers of intravenous administration.
Overlap Syndrome of Cardiac Sodium Channel Disease in Mice Carrying the Equivalent Mutation of Human <i>SCN5A</i> -1795insD
Authors: Carol Ann Remme, Arie O. Verkerk, Dieter Nuyens, Antoni C. G. van Ginneken, Sandra van Brunschot, Charly N. W. Belterman, Ronald Wilders, Marian A. van Roon, Hanno L. Tan, Arthur A. M. Wilde, Peter Carmeliet, Jacques M. T. de Bakker, Marieke W. Veldkamp, Connie R. Bezzina
Journal: Circulation (2006)

Background— Patients carrying the cardiac sodium channel ( SCN5A ) mutation 1795insD show sudden nocturnal death and signs of multiple arrhythmia syndromes including bradycardia, conduction delay, QT prolongation, and right precordial ST-elevation. We investigated the electrophysiological characteristics of a transgenic model of the murine equivalent mutation 1798insD. Methods and Results— On 24-hour continuous telemetry and surface ECG recordings, Scn5a 1798insD/+ heterozygous mice showed significantly lower heart rates, more bradycardic episodes (pauses ≥500 ms), and increased PQ interval, QRS duration, and QTc interval compared with wild-type mice. The sodium channel blocker flecainide induced marked sinus bradycardia and/or sinus arrest in the majority of Scn5a 1798insD/+ mice, but not in wild-type mice. Epicardial mapping using a multielectrode grid on excised, Langendorff-perfused hearts showed preferential conduction slowing in the right ventricle of Scn5a 1798insD/+ hearts. On whole-cell patch-clamp analysis, ventricular myocytes isolated from Scn5a 1798insD/+ hearts displayed action potential prolongation, a 39% reduction in peak sodium current density and a similar reduction in action potential upstroke velocity. Scn5a 1798insD/+ myocytes displayed a slower time course of sodium current decay without significant differences in voltage-dependence of activation and steady-state inactivation, slow inactivation, or recovery from inactivation. Furthermore, Scn5a 1798insD/+ myocytes showed a larger tetrodotoxin-sensitive persistent inward current compared with wild-type myocytes. Conclusions— Mice carrying the murine equivalent of the SCN5A -1795insD mutation display bradycardia, right ventricular conduction slowing, and QT prolongation, similar to the human phenotype. These results demonstrate that the presence of a single SCN5A mutation is indeed sufficient to cause an overlap syndrome of cardiac sodium channel disease.
Racial Differences in the Prevalence of Chronic Kidney Disease among Participants in the Reasons for Geographic and Racial Differences in Stroke (REGARDS) Cohort Study
Authors: William McClellan, David G. Warnock, Leslie McClure, Ruth C. Campbell, Britt B. Newsome, Virginia Howard, Mary Cushman, George Howard
Journal: Journal of the American Society of Nephrology (2006)

The racial disparity in the incidence of ESRD exemplified by the three- to four-fold excess risk among black compared with white individuals in the United States is not reflected in the prevalence of less severe degrees of impaired kidney function among black compared with white individuals. The four-variable Modification of Diet in Renal Disease study equation was used to evaluate the black-to-white prevalence of impaired kidney function with increasing severity of impairment among participants in the Reasons for Geographic and Racial Differences in Stroke (REGARDS) study, a nationally representative, population-based cohort of individuals who are 45 yr and older. An estimated GFR (eGFR)<60 ml/min per 1.73 m2 was present in 43.3% of the 20,667 REGARDS participants and was slightly less prevalent among black than white patients (33.7 versus 49.9%; prevalence odds ratio 0.51; 95% confidence interval [CI] 0.48 to 0.54). The lower prevalence among black patients was not uniform as eGFR declined. After controlling for other patient characteristics, the black-to-white odds ratio was 0.42 (95% CI 0.40 to 0.46) at an eGFR of 50 to 59 ml/min per 1.73 m2 and increased to 1.73 (95% CI 1.02 to 2.94) at an eGFR of 10 to 19 ml/min per 1.73 m2. The disparity in prevalence of impaired kidney function among white compared with black patients reversed as the severity of impaired kidney function increased. Factors that are responsible for the increasing prevalence of severely impaired kidney function among black patients remain to be determined.
Nerve Growth Factor–Induced Phenotypic Switch in Guinea Pig Airway Sensory Neurons
Authors: DAWN D. HUNTER, ALLEN C. MYERS, BRADLEY J. UNDEM
Journal: American Journal of Respiratory and Critical Care Medicine (2000)

Immunohistochemistry was combined with retrograde tracing techniques to characterize the effect of nerve growth factor (NGF) on substance P (SP) producing vagal neurons innervating the guinea pig trachea. Fast blue dye instilled into the trachea retrogradely labeled nerve cell bodies located in the nodose and jugular ganglia. In untreated guinea pigs > 99% of the SP-containing neurons labeled with fast blue were located in the jugular ganglia. The SP-positive neurons were small in diameter (23 ± 1 μ m) and were negative for neurofilament immunoreactivity. The fast-blue-positive neurons in the nodose ganglia, by contrast, were large in diameter (40 ± 3 μ m) and were negative for SP immunoreactivity and positive for neurofilament immunoreactivity. After NGF- β injections into the tracheal wall, approximately 10% of the large-diameter nodose neurofilament-positive neurons projecting fibers to the trachea became SP-positive (p < 0.05). We previously demonstrated that nodose nerve endings supplying the trachea are exquisitely mechanically sensitive, but capsaicin- and bradykinin-insensitive. These results suggest that NGF not only increases SP expression in airway neurons, but changes the neuronal phenotype such that large, capsaicin-insensitive nodose neurons with fast-conducting “A δ ” fibers provide a component of the tachykinergic innervation.
Lack of Agreement Between the Revised Criteria of Impaired Fasting Glucose and Impaired Glucose Tolerance in Children With Excess Body Weight
Authors: Rita Gómez-Díaz, Carlos A. Aguilar-Salinas, Segundo Morán-Villota, Rosalinda Barradas-González, Rocio Herrera-Márquez, Miguel Cruz López, Jesus Kumate, Niels H. Wacher
Journal: Diabetes Care (2004)

The aim of this study was to describe the agreement between impaired glucose tolerance (IGT) and impaired fasting glucose (IFG) in children with excess body weight using the original and the revised definitions of IFG.Obese and overweight children aged 4-17 years were included (n = 533). Anthropometric parameters and biochemical tests (fasting and 2-h glucose tests after an oral glucose load [1.75 g/kg]) were performed. Case subjects with a fasting plasma glucose >/=126 mg/dl were excluded. The diagnostic parameters of the original and the revised definitions of IFG for detecting IGT were estimated. The analysis of agreement between these categories was made using the kappa test.The prevalence of IFG increased from 6.2 to 13.3% using the new criteria. The prevalence of IFG became closer to the prevalence of IGT (14.8%). The revised criteria increased the sensitivity from 26.6 to 36.7%. However, the new IFG definition was not useful for identifying IGT cases. Of the 71 case subjects with IFG, only 29 (40.8%) had IGT. In addition, 50 case subjects with IGT (9.4%) and 13 with diabetes (2.4%) had a fasting glycemia <100 mg/dl. A poor agreement was found between the 2003 IFG definition and abnormal 2-h postchallenge plasma glucose (kappa = 0.359). The proportion of false-positive cases increased (36.3-59.1%) under the new definition.The new definition modestly increases the sensitivity of IFG for detecting IGT in children with excess body weight. Despite this, more than one-half of these cases are not detected. In addition, the false-positive rate was increased by 61%.
Triple-negative high-risk breast cancer derives particular benefit from dose intensification of adjuvant chemotherapy: results of WSG AM-01 trial
Authors: O. Gluz, U.A. Nitz, N. Harbeck, E. Ting, R. Kates, A. Herr, W. Lindemann, C. Jackisch, W.E. Berdel, H. Kirchner, B. Metzner, F. Werner, G. Schütt, M. Frick, C. Poremba, R. Diallo-Danebrock, S. Mohrmann
Journal: Annals of Oncology (2008)
Human Immunoglobulin M Memory B Cells Controlling <i>Streptococcus pneumoniae</i> Infections Are Generated in the Spleen
Authors: Stephanie Kruetzmann, M. Manuela Rosado, Holger Weber, Ulrich Germing, Olivier Tournilhac, Hans-Hartmut Peter, Reinhard Berner, Anke Peters, Thomas Boehm, Alessandro Plebani, Isabella Quinti, Rita Carsetti
Journal: The Journal of Experimental Medicine (2003)

Splenectomized and asplenic patients have a high incidence of infections by encapsulated bacteria and do not respond to polysaccharide vaccines. To understand whether the absence of the spleen is associated with a defined B cell defect, we analyzed B cell subsets in the peripheral blood. We found that a population of B cells known as immunoglobulin (Ig)M memory is lacking in patients without spleen. The absence of IgM memory B cells correlates with an impaired immune response to encapsulated bacteria not only in splenectomized patients, but also in individuals with an intact spleen. We show that the physiological and transient predisposition to pneumococcal infections of young children (0–2 yr) is associated with the lack of circulating IgM memory B cells and of serum antipolysaccharide IgM. We also demonstrate that IgM memory B cells are undetectable in a fraction of patients with common variable immunodeficiency, who have recurrent and invasive infections by encapsulated bacteria. IgM memory B cells, therefore, require the spleen for their generation and/or survival and are responsible for the protection against encapsulated bacteria.